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Information on EC 4.6.1.1 - adenylate cyclase
for references in articles please use BRENDA:EC4.6.1.1
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EC Tree 4 Lyases
4.6 Phosphorus-oxygen lyases
4.6.1 Phosphorus-oxygen lyases (only sub-subclass identified to date)
4.6.1.1 adenylate cyclase
IUBMB Comments
Also acts on dATP to form 3′,5′-cyclic dAMP. Requires pyruvate. Activated by NAD+ in the presence of EC 2.4.2.31 NAD(P)+—arginine ADP-ribosyltransferase.
The enzyme appears in viruses and cellular organisms
- 4.6.1.1
- camp
- agonist
- forskolin
-
beta-adrenergic
- pertussis
- phosphodiesterase
- isoproterenol
- prostaglandin
- gtp
- dopamine
- monophosphate
- cholera
- subtypes
- guanine
- pka
-
desensitization
- phospholipase
-
forskolin-stimulated
- g-proteins
-
camp-dependent
- epinephrine
-
pacap
- catecholamine
- parathyroid
- norepinephrine
-
adrenergic
-
muscarinic
-
vasoactive
-
guanylate
-
receptor-mediated
-
beta-adrenoceptor
-
protein-coupled
- glucagon
- bordetella
- vasopressin
-
toxin-sensitive
- naf
-
inotropic
-
gtp-binding
- 3',5'-monophosphate
- carbachol
- propranolol
-
radioligands
-
dibutyryl
- ibmx
-
adp-ribosylation
- somatostatin
- isoprenaline
- medicine
- pharmacology
- drug development
- rolipram
- 3-isobutyl-1-methylxanthine
- analysis
- molecular biology
showSynonyms
adenylate cyclase, adenylyl cyclase, adenyl cyclase, pituitary adenylate cyclase, edema factor, adenylylcyclase, soluble adenylyl cyclase, adenylate cyclase toxin, adcy5, aciii, more
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SYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
3',5'-cyclic AMP synthetase
-
-
-
-
AC
AC Rv1625c
AC toxin
AC-V
AC-VI
AC1
AC2
AC3
AC4
AC5
AC6
AC7
AC8
AC9
ACI
ACII
ACIII
ACT
ACTP10
-
-
-
-
ACV
ACVI
ADCY10
Adcy5
adenyl cyclase
-
-
-
-
adenylate cyclase
adenylate cyclase 1
adenylate cyclase 6
adenylate cyclase toxin
adenylate cyclase type 5
Adenylate cyclase, olfactive type
-
-
-
-
adenylyl cyclase
adenylyl cyclase 1
adenylyl cyclase 2
adenylyl cyclase 5
adenylyl cyclase 6
adenylyl cyclase 8
adenylyl cyclase 9
adenylyl cyclase type 1
Adenylyl cyclase type 10
-
-
-
-
adenylyl cyclase type 5
adenylyl cyclase type 8
adenylyl cyclase type V
adenylyl cyclase type VI
adenylyl cyclase, type-V
adenylyl cyclase, type-VI
adenylyl cyclase-V
adenylyl cyclase/cAMP phosphodiesterase
adenylylcyclase
-
-
-
-
ATP pyrophosphate-lyase
-
-
-
-
ATP-diphosphate-lyase cyclizing
bPAC
Ca(2+)-inhibitable adenylyl cyclase
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-
-
-
Ca(2+)/calmodulin activated adenylyl cyclase
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-
-
-
Ca-stimulated type 8 adenylyl cyclase
Ca2+-calmodulin stimulated adenylyl cyclase type 8
Ca2+-dependent adenylyl cyclase
CAPE protein
class I AC
class II AC
class III AC
class III adenylate cyclase
class III adenylyl cyclase
class IIIb AC
class IV AC
class IV adenylyl cyclase
Cya
Cya1
CyaA
CyaB
cyaB1
cyaC
cyclase, adenylate
-
-
-
-
Cyr1p
Edema factor
G protein-regulated adenylyl cyclase
HaAC
halophilic adenylate cyclase
Ma1120
mAC
membrane adenylyl cyclase
Oscil6304_3613
PAC
photoactivated adenylyl cyclase
pituitary adenylate cyclase
protein Rv0891c
Rutabaga protein
-
-
-
-
Rv0386
Rv0891c
Rv1264
Rv1318c
Rv1319c
Rv1320c
Rv1359
Rv1625c
Rv1647
Rv1900c
Rv2212
Rv2435c
Rv2488c
Rv3645
sAC
soluble AC
soluble adenylate cyclase
soluble adenylyl cyclase
STAND
ThAC
tmAC
transmembrane adenylyl cyclase
type 1 AC
type 1 adenylyl cyclase
type 1 Ca2+/calmodulin-stimulated adenylyl cyclase
type 5 adenylyl cyclase
type 6 adenylyl cyclase
type 8 AC
type III adenylyl cyclase
type VI adenylyl cyclase
xlAC
-
-
-
-
additional information
AC2
-
-
-
-
AC3
-
-
-
-
adenylyl cyclase
-
-
-
-
adenylyl cyclase
-
-
adenylyl cyclase/cAMP phosphodiesterase
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
adenylyl cyclase/cAMP phosphodiesterase
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
adenylyl cyclase/cAMP phosphodiesterase
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
adenylyl cyclase/cAMP phosphodiesterase
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
CAPE protein
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
CAPE protein
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
CAPE protein
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
CAPE protein
cf. EC 3.1.4.53, the protein encoded by this gene has a class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain
class III adenylyl cyclase
-
class III adenylyl cyclase
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33
-
class III adenylyl cyclase
-
-
Edema factor
-
-
-
-
G protein-regulated adenylyl cyclase
-
additional information
CyaA belongs to the repeats in toxin, RTX, family
additional information
the enzyme belongs to the class III adenylyl cyclase superfamily
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REACTION
REACTION DIAGRAM
COMMENTARY
ORGANISM
UNIPROT
LITERATURE
ATP = 3',5'-cyclic AMP + diphosphate
-
-
-
-
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REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
P-O bond cleavage
-
-
-
-
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SYSTEMATIC NAME
IUBMB Comments
ATP diphosphate-lyase (cyclizing; 3',5'-cyclic-AMP-forming)
Also acts on dATP to form 3',5'-cyclic dAMP. Requires pyruvate. Activated by NAD+ in the presence of EC 2.4.2.31 NAD(P)+---arginine ADP-ribosyltransferase.
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CAS REGISTRY NUMBER
COMMENTARY
9012-42-4
-
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SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
LITERATURE
COMMENTARY
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
GTP
3',5'-cyclic-GMP + diphosphate
Q7CH76
Substrates: class IV adenylyl cyclase also functions as guanylyl cyclase with about 20% efficiency
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ATP
3',5'-cAMP + diphosphate
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ATP
3',5'-cAMP + diphosphate
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ATP
3',5'-cAMP + diphosphate
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Substrates: catalytic heterodimer VC1-IIC2
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ATP
3',5'-cAMP + diphosphate
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Substrates: ACA, cAMP signalling is essential for aggregation and development of the amoebae upon starvation
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ATP
3',5'-cAMP + diphosphate
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Substrates: photoavoidance is triggered by cAMP formed by a blue-light activated class IIIb AC
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ATP
3',5'-cAMP + diphosphate
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Substrates: -
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ATP
3',5'-cAMP + diphosphate
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ATP
3',5'-cAMP + diphosphate
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Substrates: -
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ATP
3',5'-cAMP + diphosphate
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Substrates: -
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ATP
3',5'-cAMP + diphosphate
Substrates: -
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ATP
3',5'-cAMP + diphosphate
O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Substrates: -
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ATP
3',5'-cAMP + diphosphate
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Substrates: Rv1900, C-terminal CHD can use both ATP and GTP as substrate but has a 14fold preference for ATP
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ATP
3',5'-cAMP + diphosphate
Substrates: ATP substrate affinity is low
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ATP
3',5'-cAMP + diphosphate
Substrates: -
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ATP
3',5'-cAMP + diphosphate
Substrates: ATP substrate affinity is low
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ATP
3',5'-cAMP + diphosphate
Substrates: -
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ATP
3',5'-cAMP + diphosphate
Substrates: -
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ATP
3',5'-cAMP + diphosphate
Q7A2D9, Q8YVS0, Q8YMH0
Substrates: in CyaB1 only GAFB binds cAMP
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ATP
3',5'-cAMP + diphosphate
Q7A2D9, Q8YVS0, Q8YMH0
Substrates: in CyaB2 both GAFA and GAFB are cAMP receptors
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ATP
3',5'-cAMP + diphosphate
Q7A2D9, Q8YVS0, Q8YMH0
Substrates: -
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ATP
3',5'-cAMP + diphosphate
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Substrates: cAMP is required for expression of the secretion system by which virulence factors are translocated to the host cell
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ATP
3',5'-cAMP + diphosphate
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Substrates: stable co-expression of AC2 with h5-HT6 receptor in CHODUKX cell line displays dose-dependent cAMP accumulation following agonist treatment
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ATP
3',5'-cAMP + diphosphate
-
Substrates: cAMP synthesis by the AC6 isoform is not tightly coupled to cAMP hydrolysis, whereas for the other AC isoforms cAMP synthesis and hydrolysis are much more tightly linked
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ATP
3',5'-cAMP + diphosphate
-
Substrates: catalytic heterodimer VC1-IIC2
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: bifunctional protein harbouring adenylate cyclase and hemolytic activities
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: adenylyl cyclase activity results from the point mutations E497K/C566D in guanylyl cyclase
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: adenylyl cyclase activity results from the point mutations E497K/C566D in guanylyl cyclase
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
Q7A2D9
Substrates: -
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?
ATP
3',5'-cyclic AMP + diphosphate
Substrates: adenylyl cyclase also displays ion channel properties
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: adenylyl cyclase also displays ion channel properties
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: adenylyl cyclase also displays ion channel properties
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ATP
3',5'-cyclic AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: interaction with and invasion of mammalian target cells, such as monocytes and neutrophils, that express the CD11b/CD18, CR3, receptor, is facilitated by acylation of CyaA. CyaA forms small, transient, ionpermeable channels in target membranes. CyaA-induced haemolysis requires higher toxin concentrations and occurs more slowly than intoxication
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: adenylate cyclase toxin CyaA is responsible for modifications of type 2 alveolar L2 cells from flat to round form in rats after infection, overview. CyaA causes similar morphological changes in various cultured cell lines: EBL, HEK293T, MC3T3-E1, NIH 3T3, and Vero cells are rounded by the toxin, whereas Caco-2, Eph4, and MDCK cells are not. CyaA may also affect tissue cells such as respiratory epithelial cells and may be involved in the pathogenesis of the bacterial infection
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the adenylate cyclase toxin CyaA, released by Bordetella pertussis, is an essential virulence factor for colonization of the host. This toxin inhibits migration and activation of phagocytes, thereby preventing bacterial killing, and it also interferes with the initiation of adaptive immunity by misdirecting dendritic cell differentiation to a suppressive rather than stimulatory phenotype, CyaA directly affects adaptive responses by catalyzing cAMP production in human peripheral blood lymphocytes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the secreted adenylate cyclase toxin is a key virulence factor of pathogenic Bordetellae, it penetrates murine host myeloid phagocytes expressing the alphaMbeta2, e.g. J774A.1 cells, RAW 264.7 cells, or bone marrow-derived macrophage-like cells, integrin and paralyzes their bactericidal capacities by uncontrolled conversion of ATP into a key signaling molecule cAMP. cAMP signaling of CyaA causes transient and selective inactivation of RhoA in mouse macrophages in the absence of detectable activation of Rac1, Rac2, or RhoG, modeling of CyaA-mediated subversion of phagocyte functions, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: Cyr1p is a key component of the cAMP/PKA-signaling pathway that controls diverse infection-related traits, including hyphal morphogenesis
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is involved in regulation of presynaptic terminal excitability
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme, via cAMP, participates in the sugar-taste signaling pathway at the low concentration range, the long form of AC78C product is essential for the normal sugar response in adult flies, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: S103 is important for substrate binding docking to the gamma-phosphate group of ATP
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme acts as a photoreceptor for step-up photophobic response
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: most of the effects of cAMP are mediated by its receptor protein kinase A, PKA, cAMP serves as a second messenger and activates the phosphorylation enzyme PKA. The enzyme is part of the adenylyl cyclase-cyclicAMP signaling system, which is implicated in synaptic and structural plasticity and utilized by a number of neurotransmitter receptors, including serotonergic and adrenergic, to mediate their physiological functions, detailed overview. Cross-talk between the AC-cAMP and other signaling systems
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC7 is a key regulator for integration of the S1P/G13 effect on cAMP in RAW 264.7 cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the reaction is part of the cAMP signaling pathways, overview
Products: the intimate association between IP3R2 receptor and isozyme AC6 allows cAMP to pass directly from adenylate cyclase to IP3R in a manner analogous to substrate channeling in enzyme complexes, overview
Products: the intimate association between IP3R2 receptor and isozyme AC6 allows cAMP to pass directly from adenylate cyclase to IP3R in a manner analogous to substrate channeling in enzyme complexes, overview
?
ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the reaction is part of the cAMP signaling pathways, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: brains from suicide subjects show abnormalities in the cAMP signaling cascade compared to healthy subjects
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is associated to the bone mineral density and ADCY10 polymorphisms are involved in low spinal bone mineral density in hypercalciuric patients, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is involved in cAMP signaling and cAMP/PKA-mediated growth inhibition
Products: cAMP activates protein kinase A
Products: cAMP activates protein kinase A
?
ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: roles of G protein regulation of adenylyl cyclases in the brain, olfactory bulb, and heart, overview. Roles for cAMP in a vast number of biological systems, including but not limited to oogenesis, embryogenesis, larval development, hormone secretion, glycogen breakdown, smooth muscle relaxation, cardiac contraction, olfaction, and learning and memory. Physiological roles for individual adenylyl cyclase Isozymes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the C1 and C2 domains form a single ATP-binding at their interface
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cyclic AMP signaling plays a central role in regulating activity at a number of synapses in the brain, Galpha(i2) inhibition of adenylate cyclase regulates presynaptic activity and unmasks cGMP-dependent long-term depression at Schaffer collateral-CA1 hippocampal synapses, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: capacitative Ca2+ entry via plasma membrane pore-forming component Orai1, i.e. Ca2+ release-activated Ca2+ modulator 1 or CRACM1, and stromal interacting molecule 1, STIM1, regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of G protein regulation of adenylyl cyclases in the brain, olfactory bulb, and heart, overview. Roles for cAMP in a vast number of biological systems, including but not limited to oogenesis, embryogenesis, larval development, hormone secretion, glycogen breakdown, smooth muscle relaxation, cardiac contraction, olfaction, and learning and memory. Physiological roles for individual adenylyl cyclase Isozymes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the cardiac-specific isozyme AC5 plays an important role in regualting heart rate during parabolic flights, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: activation of cardiac adenylyl cyclase isozyme ACVI expression increases the function of the failing ischemic heart in mice, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina, dopamine receptor D4R activation tonically regulates the expression of AC1 in photoreceptors
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: Ca2+-dependent adenylyl cyclases play a specific role in recovery from adaptive presynaptic silencing, involvement of the cAMP pathway in the basal balance between silenced and active synapses, as well as the recovery of baseline function after depolarization-induced presynaptic silencing, e.g. by glutamate, although isozymes AC1 and AC8 are not crucial for the baseline balance between silent and active synapses, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the upregulation of fragile X mental retardation protein, FMRP, by group I metabotropic glutamate receptors, mGluRs, in anterior cingulate cortex neurons probably through cAMP response element-binding protein activation, calcium is critical for the regulation of FMRP by group I mGluRs, overview. Isozyme AC1 may contribute to the activation of CREB caused by stimulating group I mGluRs, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: cortical adenylyl cyclase 1 and activity-dependent postsynaptic AC1-cAMP signaling are required for thalamocortical synapse functional maturation and the development of normal barrel cortex cytoarchitecture, the formation of the gross morphological features of barrels is independent of postsynaptic AC1 in the layer IV barrel cortex. Regulation mechanism, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: type 1 adenylyl cyclase is essential for maintenance of remote contextual fear memory
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the upregulation of fragile X mental retardation protein, FMRP, by group I metabotropic glutamate receptors, mGluRs, in anterior cingulate cortex neurons probably through cAMP response element-binding protein activation, calcium is critical for the regulation of FMRP by group I mGluRs, overview. Isozyme AC8 may contribute to the activation of CREB caused by stimulating group I mGluRs, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the C1 and C2 domains form a single ATP-binding at their interface
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina, dopamine receptor D4R activation tonically regulates the expression of AC1 in photoreceptors
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the cardiac-specific isozyme AC5 plays an important role in regualting heart rate during parabolic flights, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: regulation of isozymes in the plasma membrane, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: capacitative Ca2+ entry via plasma membrane pore-forming component Orai1, i.e. Ca2+ release-activated Ca2+ modulator 1 or CRACM1, and stromal interacting molecule 1, STIM1, regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the enzyme is involved in beta1-AR signaling system that modulates intracellular Ca2+ in the heart. The enzyme is involved in mediation of the antiarrhymthmic effect of electro-acupuncture in the heart, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: interaction of mu-opioid receptors with G proteins and adenylyl cyclase in lumbar segments of the spinal cord, regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: soluble isozymes sAC play a unique function in male germ cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: regulation of epithelial Na+ transport by soluble adenylyl cyclase in kidney collecting duct cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the enzyme is one of the signal transducing systems implicated in the regulation of the cardiovascular system and plays a role in signaling in vascular smooth muscle cells, which is decreased by oxidative stress, induced by high glucose, along with the expression of Gialpha proteins, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: Ca2+-dependent adenylyl cyclases play a specific role in recovery from adaptive presynaptic silencing, involvement of the cAMP pathway in the basal balance between silenced and active synapses, as well as the recovery of baseline function after depolarization-induced presynaptic silencing, e.g. by glutamate, although isozymes AC1 and AC8 are not crucial for the baseline balance between silent and active synapses, overview. But AC8 plays a particularly important role in rapidly resetting the balance of active to silent synapses after adaptation to strong activity
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the soluble adenylyl cyclase is the main producer of glucose-induced cAMP in INS-1E insulinoma cells, while the transmembrane adenylyl cyclase does not play a role, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: adenylate cyclase-activating polypeptide type 1 receptor, PAC1-R, is involved in cAMP signalling in the pituitary gland
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme modulates the cardiovascular response of posterior hypothalamic adenosine A2A receptor stimulation, adenylate cyclase, but not guanylate cyclase, mediates the depressor and bradycardiac actions of adenosine A2A receptors, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the adenylyl cyclase signaling cascade is involved in nicotine dependence and withdrawal, but also mediates numerous other neurotransmitter responses, effects of nicotine on adenylate cyclase enzyme activity: adolescent nicotine exposure elicits persistent suppression of basal adenylate cyclase activity and eventual compromise of responses to beta-adrenergic receptor stimulation, with effects emerging in late adulthood, overview
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
-
Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: SAC1 acts downstream of heterotrimeric G protein GSA3, parallel to a GSA1-GSA2-mediated signaling pathway
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ATP
cAMP + diphosphate
Substrates: -
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additional information
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-
Substrates: development of a method for fluorimetric assay for real-time monitoring of adenylyl cyclase activity based on terbium norfloxacin, evaluation, application of radioactively labeled substrate, such as [a-32P]ATP, or fluorescently labeled antibodies, overview
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additional information
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Substrates: there may be ecological niches in which CyaA is not critical for the success of Bordetella bronchiseptica
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additional information
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Substrates: at high toxin concentrations, non-acylated CyaA can intoxicate macrophages by delivery of the catalytic domain. CyaA, but not mutant CyaA*, is able to induce caspase 3/7 activity, CyaA causes 50% inhibition of the zymosan-stimulated oxidative burst
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additional information
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Substrates: at high toxin concentrations, non-acylated CyaA can intoxicate macrophages by delivery of the catalytic domain. CyaA, but not mutant CyaA*, is able to induce caspase 3/7 activity, CyaA causes 50% inhibition of the zymosan-stimulated oxidative burst
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additional information
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Substrates: CyaA increases the cAMP level and activates PKA in human host T lymphocytes, treatment of human T-lymphocytes with CyaA results in profound impairment of T-lymphocyte activation and chemotaxis, caused by inhibition of T-cell antigen receptor and chemokine receptor signaling via a cAMP/protein kinase A-dependent pathway, overview. The biological effects of the toxin are paralleled by inhibition of the activation of mitogen-activated protein kinases
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additional information
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Substrates: the CyaA/cAMP-induced drop of RhoA activity yielded dephosphorylation of the actinfilament severing protein cofilin and massive actin cytoskeleton rearrangements, which were paralleled by rapidly manifested macrophage ruffling and a rapid and unexpected loss of macropinocytic fluid phase uptake. CyaA/cAMP signaling further caused a rapid and near-complete block of complement-mediated phagocytosis. CyaA-induced membrane ruffling in host cells is transient and wanes faster at higher toxin concentration, overview
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: Ras1p and Cyr1p work as a complex that constitutes part of a sensor/effector machinery, and their interaction ensures proper protein folding for optimal ligand sensing and/or subsequent allosteric activation of the catalytic domain, without Ras1p the system functions partially, thereby requiring strong inducing signals to activate downstream events for hyphal growth, overview
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additional information
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Substrates: the A2B adenosine receptor controls at least three independent signaling pathways, one of which is the Gs-mediated stimulation of adenylate cyclase, in mast cells and microvascular endothelial cells
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additional information
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Substrates: structure-function relationship, overview
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additional information
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Substrates: structure-function relationship, overview
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additional information
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Substrates: enzyme HpAC1 has substantial triphosphatase activity, the strongest NTPase activity of HpAC1 is observed at pH 9.5 with GTP
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additional information
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Substrates: adenylyl cyclase and cAMP formation in mood disorders and the role of the enzyme protein kinase A, mood disorders are among the most prevalent and recurrent forms of psychiatric illnesses, mechanistic basics, overview. In depressed patients, the expression of stimulatory G protein is increased and of inhibitory G protein is decreased, which suggests greater stimulation of the cAMP pathway
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additional information
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Substrates: the A2B adenosine receptor controls at least three independent signaling pathways, one of which is the Gs-mediated stimulation of adenylate cyclase, in mast cells and microvascular endothelial cells
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview. Overexpression of Galpha12/13QL is unlikely to regulate the activity of Gs, rather it acts to attenuate the G13 pathway that converges on AC7
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview. Overexpression of Galpha12/13QL is unlikely to regulate the activity of Gs, rather it acts to attenuate the G13 pathway that converges on AC7
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: sickle red cell adhesion contributes to sickle cell disease pathophysiology, involving the gene interaction of gene ADCY6, encoding the adenylate cyclase, and gene ADRB2, encoding the beta2-adrenergic receptor, altered interaction affects sickel red cell adhesion to laminin, overview
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additional information
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Substrates: reduction of adenylyl cyclase activity induced by NaF and the increase in the Gi/Gs ratio could explain the changes in neurotransmission in humans with depression
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additional information
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Substrates: Epstein Barr virus infection of B-lymphocyte renders the cells resistent against to cAMP/PKA-mediated growth inhibition, and the infection abolishes enzyme activation by forskolin, NaF, and G proteins, and the ability of forskolin to inhibit camptothecin-induced apoptosis, and it abolishes the inhibitory effect of forskolin on apoptosis induced by S phase-specific cytotoxic drugs, overview
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additional information
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Substrates: optimization of a radioimmunoassay method for cAMP, with markedly improved speed and reduced cost without sacrificing sensitivity, and also adaptable to analysis of cGMP. Development of a simple, reproducible, and inexpensive method to make the radiomarker used for the radioimmunoassay, overview
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additional information
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Substrates: FSK-dependent cAMP generation measured in wild-type and FSK-site mutants by biosensor-based live cell assay
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additional information
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Substrates: adenylyl cyclase activity is measured using terbium norfloxacin assay
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: the complexity of signalling by the ubiquitous second messenger cAMP is enhanced by multiple regulatory susceptibilities of its synthesis by adenylyl cyclases and degradation by phosphodiesterases, ACs receive regulatory signals from multiple sources, such as G-proteins, protein kinases, growth factors and Ca2+
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additional information
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Substrates: inhibition of adenylyl cyclase and cAMP production is involved in somatostatin anti-angiogenic actions, neoangiogenesis is a response to retinal hypoxia that is inhibited by somatostatin through its subtype 2 receptor, sst2, hypoxia increases AC responsiveness, especially of isozyme ACVII, in wild-type retinas and in retinas lacking sst2, but not in sst2-overexpressing retinas, overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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additional information
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Substrates: soluble adenylyl cyclase is an essential component of cAMP-signalling cascades that activate sperm motility and capacitate sperm, but soluble adenylyl cyclase does not have a direct effect on hyperactivation
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additional information
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Substrates: the light- and dopamine D4 receptor-signaling pathways converge on the type 1 Ca2+/calmodulin-stimulated adenylyl cyclase to regulate cyclic AMP synthesis in photoreceptor cells, essential roles of D4 receptors and AC1 in photic control of cyclic AMP in photoreceptor cells, overview
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additional information
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Substrates: adenylyl cyclase-5 activity in the nucleus accumbens regulates anxiety-related behavior, overview
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additional information
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Substrates: netrin-1 does not alter cAMP levels in axons attracted by this cue, and soluble adenylyl cyclase is not required for axon guidance to netrin-1
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additional information
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Substrates: AC1 is expressed throughout the trigeminal pathway
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additional information
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Substrates: concomitant activation of adenylyl cyclase suppresses the opposite influences of CB1 cannabinoid receptor agonists on tyrosine hydroxylase expression, overview
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additional information
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: the light- and dopamine D4 receptor-signaling pathways converge on the type 1 Ca2+/calmodulin-stimulated adenylyl cyclase to regulate cyclic AMP synthesis in photoreceptor cells, essential roles of D4 receptors and AC1 in photic control of cyclic AMP in photoreceptor cells, overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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additional information
?
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Substrates: concomitant activation of adenylyl cyclase suppresses the opposite influences of CB1 cannabinoid receptor agonists on tyrosine hydroxylase expression, overview
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additional information
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Substrates: measurement of the ATPase activity of the enzyme
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additional information
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Substrates: measurement of the ATPase activity of the enzyme
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additional information
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Substrates: measurement of the ATPase activity of the enzyme
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through rodent host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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additional information
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through human host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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additional information
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through rodent host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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additional information
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Substrates: the transmembrane isozymes is regulated by forskolin and G proteins, while the soluble isozyme is insensitive
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additional information
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Substrates: the complexity of signalling by the ubiquitous second messenger cAMP is enhanced by multiple regulatory susceptibilities of its synthesis by adenylyl cyclases and degradation by phosphodiesterases, ACs receive regulatory signals from multiple sources, such as G-proteins, protein kinases, growth factors and Ca2+
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additional information
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Substrates: the mu-opioid selective agonists, sufentanil and DAMGO, stimulate 5'-(gamma-thio)-triphosphate binding and inhibit forskolin-stimulated adenylyl cyclase activity, through a mechanism involving pertussis toxin, PTX, sensitive Gai/o subunits, the enhanced analgesic response following combined nimodipine treatment with sufentanil is associated with adenylyl cyclase supersensitivity to the opioid inhibitory effect through a mechanism involving PTX-resistant G protein subunits, overview
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additional information
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Substrates: soluble adenylyl cyclase inhibition blocks ATPase activity without affecting surface expression of the Na+ pump
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additional information
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Substrates: netrin-1 does not alter cAMP levels in axons attracted by this cue, and soluble adenylyl cyclase is not required for axon guidance to netrin-1
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additional information
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Substrates: the pituitary adenylate cyclase-activating polypeptide type 1 receptor, PAC1-R, a member of the 7-transmembrane domain, group 2 G-protein coupled receptor family, modulate neurotransmission and neurotrophic actions, its activation is pronociceptive. Blockade of the PAC1-R/PACAP complex by PACAP 6-38, a PAC1-R antagonist, can effectively attenuate thermal hyperalgesia and mechanical allodynia associated with inflammatory and neuropathic pain states, overview
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additional information
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Substrates: reduction of adenylyl cyclase activity induced by NaF and the increase in the Gi/Gs ratio can explain the changes in neurotransmission in olfactory bulbectomy rats, overview. Two weeks after surgery and compared to sham controls, olfactory bulbectomy rats display reduced NaF-stimulated adenylyl cyclase activity and increased Gi/Gs ratios in the hypothalamus, pre-frontal and cingulate cortices but not in the amygdala, hippocampus and caudate nucleus. No differences are found in basal or forskolin-stimulated conditions
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Q7CH76
Substrates: class IV adenylyl cyclase also functions as guanylyl cyclase
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additional information
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Substrates: class IV adenylyl cyclase also functions as guanylyl cyclase
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NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
LITERATURE
COMMENTARY
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
ATP
3',5'-cyclic AMP + diphosphate
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Substrates: bifunctional protein harbouring adenylate cyclase and hemolytic activities
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
Q7A2D9
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: interaction with and invasion of mammalian target cells, such as monocytes and neutrophils, that express the CD11b/CD18, CR3, receptor, is facilitated by acylation of CyaA. CyaA forms small, transient, ionpermeable channels in target membranes. CyaA-induced haemolysis requires higher toxin concentrations and occurs more slowly than intoxication
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: adenylate cyclase toxin CyaA is responsible for modifications of type 2 alveolar L2 cells from flat to round form in rats after infection, overview. CyaA causes similar morphological changes in various cultured cell lines: EBL, HEK293T, MC3T3-E1, NIH 3T3, and Vero cells are rounded by the toxin, whereas Caco-2, Eph4, and MDCK cells are not. CyaA may also affect tissue cells such as respiratory epithelial cells and may be involved in the pathogenesis of the bacterial infection
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the adenylate cyclase toxin CyaA, released by Bordetella pertussis, is an essential virulence factor for colonization of the host. This toxin inhibits migration and activation of phagocytes, thereby preventing bacterial killing, and it also interferes with the initiation of adaptive immunity by misdirecting dendritic cell differentiation to a suppressive rather than stimulatory phenotype, CyaA directly affects adaptive responses by catalyzing cAMP production in human peripheral blood lymphocytes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the secreted adenylate cyclase toxin is a key virulence factor of pathogenic Bordetellae, it penetrates murine host myeloid phagocytes expressing the alphaMbeta2, e.g. J774A.1 cells, RAW 264.7 cells, or bone marrow-derived macrophage-like cells, integrin and paralyzes their bactericidal capacities by uncontrolled conversion of ATP into a key signaling molecule cAMP. cAMP signaling of CyaA causes transient and selective inactivation of RhoA in mouse macrophages in the absence of detectable activation of Rac1, Rac2, or RhoG, modeling of CyaA-mediated subversion of phagocyte functions, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: Cyr1p is a key component of the cAMP/PKA-signaling pathway that controls diverse infection-related traits, including hyphal morphogenesis
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is involved in regulation of presynaptic terminal excitability
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme, via cAMP, participates in the sugar-taste signaling pathway at the low concentration range, the long form of AC78C product is essential for the normal sugar response in adult flies, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme acts as a photoreceptor for step-up photophobic response
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: most of the effects of cAMP are mediated by its receptor protein kinase A, PKA, cAMP serves as a second messenger and activates the phosphorylation enzyme PKA. The enzyme is part of the adenylyl cyclase-cyclicAMP signaling system, which is implicated in synaptic and structural plasticity and utilized by a number of neurotransmitter receptors, including serotonergic and adrenergic, to mediate their physiological functions, detailed overview. Cross-talk between the AC-cAMP and other signaling systems
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC7 is a key regulator for integration of the S1P/G13 effect on cAMP in RAW 264.7 cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the reaction is part of the cAMP signaling pathways, overview
Products: the intimate association between IP3R2 receptor and isozyme AC6 allows cAMP to pass directly from adenylate cyclase to IP3R in a manner analogous to substrate channeling in enzyme complexes, overview
Products: the intimate association between IP3R2 receptor and isozyme AC6 allows cAMP to pass directly from adenylate cyclase to IP3R in a manner analogous to substrate channeling in enzyme complexes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the reaction is part of the cAMP signaling pathways, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: brains from suicide subjects show abnormalities in the cAMP signaling cascade compared to healthy subjects
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is associated to the bone mineral density and ADCY10 polymorphisms are involved in low spinal bone mineral density in hypercalciuric patients, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is involved in cAMP signaling and cAMP/PKA-mediated growth inhibition
Products: cAMP activates protein kinase A
Products: cAMP activates protein kinase A
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: roles of G protein regulation of adenylyl cyclases in the brain, olfactory bulb, and heart, overview. Roles for cAMP in a vast number of biological systems, including but not limited to oogenesis, embryogenesis, larval development, hormone secretion, glycogen breakdown, smooth muscle relaxation, cardiac contraction, olfaction, and learning and memory. Physiological roles for individual adenylyl cyclase Isozymes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cyclic AMP signaling plays a central role in regulating activity at a number of synapses in the brain, Galpha(i2) inhibition of adenylate cyclase regulates presynaptic activity and unmasks cGMP-dependent long-term depression at Schaffer collateral-CA1 hippocampal synapses, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: capacitative Ca2+ entry via plasma membrane pore-forming component Orai1, i.e. Ca2+ release-activated Ca2+ modulator 1 or CRACM1, and stromal interacting molecule 1, STIM1, regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of G protein regulation of adenylyl cyclases in the brain, olfactory bulb, and heart, overview. Roles for cAMP in a vast number of biological systems, including but not limited to oogenesis, embryogenesis, larval development, hormone secretion, glycogen breakdown, smooth muscle relaxation, cardiac contraction, olfaction, and learning and memory. Physiological roles for individual adenylyl cyclase Isozymes, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the cardiac-specific isozyme AC5 plays an important role in regualting heart rate during parabolic flights, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: activation of cardiac adenylyl cyclase isozyme ACVI expression increases the function of the failing ischemic heart in mice, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina, dopamine receptor D4R activation tonically regulates the expression of AC1 in photoreceptors
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: Ca2+-dependent adenylyl cyclases play a specific role in recovery from adaptive presynaptic silencing, involvement of the cAMP pathway in the basal balance between silenced and active synapses, as well as the recovery of baseline function after depolarization-induced presynaptic silencing, e.g. by glutamate, although isozymes AC1 and AC8 are not crucial for the baseline balance between silent and active synapses, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the upregulation of fragile X mental retardation protein, FMRP, by group I metabotropic glutamate receptors, mGluRs, in anterior cingulate cortex neurons probably through cAMP response element-binding protein activation, calcium is critical for the regulation of FMRP by group I mGluRs, overview. Isozyme AC1 may contribute to the activation of CREB caused by stimulating group I mGluRs, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cortical adenylyl cyclase 1 and activity-dependent postsynaptic AC1-cAMP signaling are required for thalamocortical synapse functional maturation and the development of normal barrel cortex cytoarchitecture, the formation of the gross morphological features of barrels is independent of postsynaptic AC1 in the layer IV barrel cortex. Regulation mechanism, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: type 1 adenylyl cyclase is essential for maintenance of remote contextual fear memory
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: -
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the upregulation of fragile X mental retardation protein, FMRP, by group I metabotropic glutamate receptors, mGluRs, in anterior cingulate cortex neurons probably through cAMP response element-binding protein activation, calcium is critical for the regulation of FMRP by group I mGluRs, overview. Isozyme AC8 may contribute to the activation of CREB caused by stimulating group I mGluRs, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina, dopamine receptor D4R activation tonically regulates the expression of AC1 in photoreceptors
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: the cardiac-specific isozyme AC5 plays an important role in regualting heart rate during parabolic flights, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: regulation of isozymes in the plasma membrane, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: capacitative Ca2+ entry via plasma membrane pore-forming component Orai1, i.e. Ca2+ release-activated Ca2+ modulator 1 or CRACM1, and stromal interacting molecule 1, STIM1, regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, detailed overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is involved in beta1-AR signaling system that modulates intracellular Ca2+ in the heart. The enzyme is involved in mediation of the antiarrhymthmic effect of electro-acupuncture in the heart, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: interaction of mu-opioid receptors with G proteins and adenylyl cyclase in lumbar segments of the spinal cord, regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: soluble isozymes sAC play a unique function in male germ cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: regulation of epithelial Na+ transport by soluble adenylyl cyclase in kidney collecting duct cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is one of the signal transducing systems implicated in the regulation of the cardiovascular system and plays a role in signaling in vascular smooth muscle cells, which is decreased by oxidative stress, induced by high glucose, along with the expression of Gialpha proteins, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: Ca2+-dependent adenylyl cyclases play a specific role in recovery from adaptive presynaptic silencing, involvement of the cAMP pathway in the basal balance between silenced and active synapses, as well as the recovery of baseline function after depolarization-induced presynaptic silencing, e.g. by glutamate, although isozymes AC1 and AC8 are not crucial for the baseline balance between silent and active synapses, overview. But AC8 plays a particularly important role in rapidly resetting the balance of active to silent synapses after adaptation to strong activity
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the soluble adenylyl cyclase is the main producer of glucose-induced cAMP in INS-1E insulinoma cells, while the transmembrane adenylyl cyclase does not play a role, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: adenylate cyclase-activating polypeptide type 1 receptor, PAC1-R, is involved in cAMP signalling in the pituitary gland
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme modulates the cardiovascular response of posterior hypothalamic adenosine A2A receptor stimulation, adenylate cyclase, but not guanylate cyclase, mediates the depressor and bradycardiac actions of adenosine A2A receptors, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the adenylyl cyclase signaling cascade is involved in nicotine dependence and withdrawal, but also mediates numerous other neurotransmitter responses, effects of nicotine on adenylate cyclase enzyme activity: adolescent nicotine exposure elicits persistent suppression of basal adenylate cyclase activity and eventual compromise of responses to beta-adrenergic receptor stimulation, with effects emerging in late adulthood, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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Substrates: the enzyme is a key component of the adenylate cyclase signaling system, mechanism and regulation, overview
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ATP
3',5'-cyclic-AMP + diphosphate
Substrates: SAC1 acts downstream of heterotrimeric G protein GSA3, parallel to a GSA1-GSA2-mediated signaling pathway
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additional information
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Substrates: there may be ecological niches in which CyaA is not critical for the success of Bordetella bronchiseptica
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additional information
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Substrates: at high toxin concentrations, non-acylated CyaA can intoxicate macrophages by delivery of the catalytic domain. CyaA, but not mutant CyaA*, is able to induce caspase 3/7 activity, CyaA causes 50% inhibition of the zymosan-stimulated oxidative burst
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additional information
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Substrates: at high toxin concentrations, non-acylated CyaA can intoxicate macrophages by delivery of the catalytic domain. CyaA, but not mutant CyaA*, is able to induce caspase 3/7 activity, CyaA causes 50% inhibition of the zymosan-stimulated oxidative burst
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Substrates: CyaA increases the cAMP level and activates PKA in human host T lymphocytes, treatment of human T-lymphocytes with CyaA results in profound impairment of T-lymphocyte activation and chemotaxis, caused by inhibition of T-cell antigen receptor and chemokine receptor signaling via a cAMP/protein kinase A-dependent pathway, overview. The biological effects of the toxin are paralleled by inhibition of the activation of mitogen-activated protein kinases
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additional information
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Substrates: the CyaA/cAMP-induced drop of RhoA activity yielded dephosphorylation of the actinfilament severing protein cofilin and massive actin cytoskeleton rearrangements, which were paralleled by rapidly manifested macrophage ruffling and a rapid and unexpected loss of macropinocytic fluid phase uptake. CyaA/cAMP signaling further caused a rapid and near-complete block of complement-mediated phagocytosis. CyaA-induced membrane ruffling in host cells is transient and wanes faster at higher toxin concentration, overview
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: Ras1p and Cyr1p work as a complex that constitutes part of a sensor/effector machinery, and their interaction ensures proper protein folding for optimal ligand sensing and/or subsequent allosteric activation of the catalytic domain, without Ras1p the system functions partially, thereby requiring strong inducing signals to activate downstream events for hyphal growth, overview
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additional information
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Substrates: the A2B adenosine receptor controls at least three independent signaling pathways, one of which is the Gs-mediated stimulation of adenylate cyclase, in mast cells and microvascular endothelial cells
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additional information
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Substrates: adenylyl cyclase and cAMP formation in mood disorders and the role of the enzyme protein kinase A, mood disorders are among the most prevalent and recurrent forms of psychiatric illnesses, mechanistic basics, overview. In depressed patients, the expression of stimulatory G protein is increased and of inhibitory G protein is decreased, which suggests greater stimulation of the cAMP pathway
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additional information
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Substrates: the A2B adenosine receptor controls at least three independent signaling pathways, one of which is the Gs-mediated stimulation of adenylate cyclase, in mast cells and microvascular endothelial cells
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview. Overexpression of Galpha12/13QL is unlikely to regulate the activity of Gs, rather it acts to attenuate the G13 pathway that converges on AC7
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview. Overexpression of Galpha12/13QL is unlikely to regulate the activity of Gs, rather it acts to attenuate the G13 pathway that converges on AC7
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview
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additional information
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Substrates: a synergism between the Gs and G13 pathways, mediated by the S1P2 receptor and the heterotrimeric G protein G13, occurs through regulation of a specific isoform of adenylyl cyclase, G13 regulation of AC7 activity is mediated by its alpha-subunit, overview
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: potentiation of IP3-evoked Ca2+-signals by PTH specifically requires AC6 and IP3R2 receptor, the muscarinic receptors, that alone evoke Ca2+ release, are distributed differently to those that release Ca2+ in synergy with cAMP, overview. Focal inhibition of the enzyme more effectively inhibits Ca2+ signaling than global inhibition
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additional information
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Substrates: sickle red cell adhesion contributes to sickle cell disease pathophysiology, involving the gene interaction of gene ADCY6, encoding the adenylate cyclase, and gene ADRB2, encoding the beta2-adrenergic receptor, altered interaction affects sickel red cell adhesion to laminin, overview
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additional information
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Substrates: reduction of adenylyl cyclase activity induced by NaF and the increase in the Gi/Gs ratio could explain the changes in neurotransmission in humans with depression
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additional information
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Substrates: Epstein Barr virus infection of B-lymphocyte renders the cells resistent against to cAMP/PKA-mediated growth inhibition, and the infection abolishes enzyme activation by forskolin, NaF, and G proteins, and the ability of forskolin to inhibit camptothecin-induced apoptosis, and it abolishes the inhibitory effect of forskolin on apoptosis induced by S phase-specific cytotoxic drugs, overview
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additional information
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Substrates: FSK-dependent cAMP generation measured in wild-type and FSK-site mutants by biosensor-based live cell assay
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: the complexity of signalling by the ubiquitous second messenger cAMP is enhanced by multiple regulatory susceptibilities of its synthesis by adenylyl cyclases and degradation by phosphodiesterases, ACs receive regulatory signals from multiple sources, such as G-proteins, protein kinases, growth factors and Ca2+
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Substrates: inhibition of adenylyl cyclase and cAMP production is involved in somatostatin anti-angiogenic actions, neoangiogenesis is a response to retinal hypoxia that is inhibited by somatostatin through its subtype 2 receptor, sst2, hypoxia increases AC responsiveness, especially of isozyme ACVII, in wild-type retinas and in retinas lacking sst2, but not in sst2-overexpressing retinas, overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of adenylate cyclase is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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Substrates: soluble adenylyl cyclase is an essential component of cAMP-signalling cascades that activate sperm motility and capacitate sperm, but soluble adenylyl cyclase does not have a direct effect on hyperactivation
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Substrates: the light- and dopamine D4 receptor-signaling pathways converge on the type 1 Ca2+/calmodulin-stimulated adenylyl cyclase to regulate cyclic AMP synthesis in photoreceptor cells, essential roles of D4 receptors and AC1 in photic control of cyclic AMP in photoreceptor cells, overview
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Substrates: adenylyl cyclase-5 activity in the nucleus accumbens regulates anxiety-related behavior, overview
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Substrates: netrin-1 does not alter cAMP levels in axons attracted by this cue, and soluble adenylyl cyclase is not required for axon guidance to netrin-1
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Substrates: AC1 is expressed throughout the trigeminal pathway
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Substrates: concomitant activation of adenylyl cyclase suppresses the opposite influences of CB1 cannabinoid receptor agonists on tyrosine hydroxylase expression, overview
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: key to regulation of AC is the interface between the C1 and C2 domains which forms a single ATP-binding site, regulatory patterns and mechanisms for the various isozyme groups, detailed overview
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additional information
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Substrates: the light- and dopamine D4 receptor-signaling pathways converge on the type 1 Ca2+/calmodulin-stimulated adenylyl cyclase to regulate cyclic AMP synthesis in photoreceptor cells, essential roles of D4 receptors and AC1 in photic control of cyclic AMP in photoreceptor cells, overview
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additional information
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Substrates: type 5 adenylyl cyclase plays a major role in stabilizing heart rate in response to microgravity induced by parabolic flight, overview
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additional information
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Substrates: concomitant activation of adenylyl cyclase suppresses the opposite influences of CB1 cannabinoid receptor agonists on tyrosine hydroxylase expression, overview
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additional information
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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additional information
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through rodent host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through human host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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Substrates: increases in cAMP in sporozoites are required for apical regulated exocytosis for migration through rodent host liver cells, exocytosis with increased cAMP levels reduces sporozoite migration through host cells, confirming that such extensive migration is no longer necessary when exocytosis is induced by elevations in the level of cAMP, overview
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Substrates: the transmembrane isozymes is regulated by forskolin and G proteins, while the soluble isozyme is insensitive
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Substrates: the complexity of signalling by the ubiquitous second messenger cAMP is enhanced by multiple regulatory susceptibilities of its synthesis by adenylyl cyclases and degradation by phosphodiesterases, ACs receive regulatory signals from multiple sources, such as G-proteins, protein kinases, growth factors and Ca2+
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Substrates: the mu-opioid selective agonists, sufentanil and DAMGO, stimulate 5'-(gamma-thio)-triphosphate binding and inhibit forskolin-stimulated adenylyl cyclase activity, through a mechanism involving pertussis toxin, PTX, sensitive Gai/o subunits, the enhanced analgesic response following combined nimodipine treatment with sufentanil is associated with adenylyl cyclase supersensitivity to the opioid inhibitory effect through a mechanism involving PTX-resistant G protein subunits, overview
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Substrates: soluble adenylyl cyclase inhibition blocks ATPase activity without affecting surface expression of the Na+ pump
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additional information
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Substrates: netrin-1 does not alter cAMP levels in axons attracted by this cue, and soluble adenylyl cyclase is not required for axon guidance to netrin-1
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Substrates: the pituitary adenylate cyclase-activating polypeptide type 1 receptor, PAC1-R, a member of the 7-transmembrane domain, group 2 G-protein coupled receptor family, modulate neurotransmission and neurotrophic actions, its activation is pronociceptive. Blockade of the PAC1-R/PACAP complex by PACAP 6-38, a PAC1-R antagonist, can effectively attenuate thermal hyperalgesia and mechanical allodynia associated with inflammatory and neuropathic pain states, overview
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Substrates: reduction of adenylyl cyclase activity induced by NaF and the increase in the Gi/Gs ratio can explain the changes in neurotransmission in olfactory bulbectomy rats, overview. Two weeks after surgery and compared to sham controls, olfactory bulbectomy rats display reduced NaF-stimulated adenylyl cyclase activity and increased Gi/Gs ratios in the hypothalamus, pre-frontal and cingulate cortices but not in the amygdala, hippocampus and caudate nucleus. No differences are found in basal or forskolin-stimulated conditions
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Substrates: plant soluble adenylyl cyclases are part of a complex signaling system affected by biotic and abiotic factors, e.g. low temperature, phytohormones, biogenic inductors, light, viruses, and bacterial metabolites
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COFACTOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
additional information
membrane-anchored adenylyl cyclase isoform 9 (AC9) is conditionally activated by the heterotrimeric G protein Gbetagamma
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Calmodulin
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activation
Calmodulin
-
CyaA binds calmodulin that stimulates about 1000fold its enzymatic activity
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METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
bicarbonate
Ca2+
Co2+
Cu2+
-
stimulation of enzyme activity at nanomolar concentrations, strong inhibition in the micromolar range
F-
Fe2+
HCO3-
Mg2+
Mn2+
Zn2+
additional information
Ca2+
-
requirement for dual regulation of the AC by both Gs activation and Ca2+/calmodulin in a time-dependent manner
Ca2+
CyaA is a calcium-binding protein, Ca2+ binding leads a a rearrangement of the enzyme's secondary structure, overview
Ca2+
-
half-maximal activation at 0.75 mM, synergistic activation in the presence of HCO3-
Ca2+
-
during artificial or agonist-induced Ca2+ oscillations, periodic changes in cAMP that depended upon Ca2+ stimulation of AC8 with subsequent PKA-mediated phosphodiesterase 4 activity
Ca2+
-
the isozyme group I consists of Ca 2+ -stimulated AC1, AC3 and AC8, isozyme group III is comprised of Gialpha /Ca2+ -inhibited isozymes AC5 and AC6, mode of regulation, overview
Ca2+
-
required by AC1 and AC8, AC1 is sensitive to lower concentrations of Ca2+ and shows a greater synergistic response to Ca2+ and Galphas than does AC8
Ca2+
-
stimulates Ca2+ stimulates transmembrane isozymes AC1 and AC8 via calmodulin, and inhibits AC5 and AC6 directly, capacitative Ca2+ entry via Orai1 and STIM1 regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, AC8 shows a dis-inhibitory activation mechanism
Ca2+
-
isozymes AC1 and AC8 are the major Ca2+-sensitive AC isoforms, generally ubiquitous role of Ca2+ in the induction of activity-dependent synaptic plasticity
Ca2+
-
AC1 and the formation of cAMP,are stimulated by increases in intracellular Ca2+ levels in an activity-dependent manner
Ca2+
isozyme group III is comprised of Gialpha /Ca2+ -inhibited isozymes AC5 and AC6, mode of regulation, overview
Ca2+
the isozyme group I consists of Ca2+-stimulated AC1, AC3 and AC8, mode of regulation, overview
Ca2+
the isozyme group I consists of Ca2+-stimulated AC8, mode of regulation, overview
Ca2+
isozyme group III is comprised of Gialpha /Ca2+-inhibited isozymes AC5 and AC6, mode of regulation, overview
Ca2+
the isozyme group I consists of Ca2+-stimulated isozymes AC1, AC3 and AC8, mode of regulation, overview
Ca2+
-
L-type Ca2+ channel interacting with signaling proteins like adenylate cyclase, to create a large signaling complex that provides rapid and specific signaling of Cav1.2 during beta2-AR activation
Ca2+
-
isozymes AC1 and AC8 are the major Ca2+-sensitive AC isoforms, generally ubiquitous role of Ca2+ in the induction of activity-dependent synaptic plasticity
Ca2+
Ca2+ stimulates transmembrane isozyme AC8 via calmodulin, capacitative Ca2+ entry via Orai1 and STIM1 regulates adenylyl cyclase type 8, other modes of Ca2+ entry, including those activated by arachidonate and the ionophore ionomycin, are ineffective, AC8 shows a dis-inhibitory activation mechanism
Ca2+
-
maximum stimulatory effect at 0.002 mM Ca2+. (increase of 387% activity). Antagonists of calmodulin, N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride, at concentrations of 0.02-0.1 mM decrease the stimulatory effect of 0.005 mM Ca2+, while at the higher concentrations inhibit it completely. Chloropromazine decreases the Ca2+-stimulated adenylyl cyclase activity only at concentrations of 0.2-1.0 mM
Mg2+
-
10 mM, 19fold increase in activity, recombinant CyaB1-maltose binding protein fusion
Mg2+
the class I enzyme shows a requirement for free metal ions in addition to the MgATP2- complex, operating with a two-metal-ion mechanism in analogy to class II and calss III enzymes. The native enzyme shows very little activity when the concentration of Mg2+ is much lower than that of ATP, and activity rises strongly when the concentration of Mg2+ exceeds that of ATP
Mg2+
-
Mg2+ is the physiological cation involved in adenylyl cyclase enzyme activity
Mg2+
2 mM required for activity, recombinant AC expressed from synthetic AC gene PfAC526-884
Mg2+
-
Mg2+ is required for forskolin-dependent accumulation of cAMP, best at 1-3 mM
Mg2+
-
about 50fold lower enzyme activity than in the presence of Mn2+
Mn2+
-
10 mM, 50fold increase in activity, recombinant CyaB1-maltose binding protein fusion
Mn2+
-
highly activating for the AC activity also activates the phosphohydrolase activity
Mn2+
-
activates, required for catalysis. Production of cAMP by His-tagged isozyme rtsACT is increased approximately 20fold by 5 mM Mn2+
Mn2+
-
required, the enzyme has higher specific activity for Mn2+-ATP versus Mg2+-ATP
Mn2+
Q7CH76
the wild type enzyme is about 2.5fold more active with saturating Mg2+ than with saturating Mn2+
additional information
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the basal activity of isoform AC3 does not change in the presence of Ca2+ or Ca2+/calmodulin
additional information
-
no metals bound in the structure of the c-diGMP-bound PleD complex
additional information
Ca2+ can fully inhibit the PPPase activity, whereas Mn2+ inhibition yields a residual activity of about 9 %
additional information
-
as metalloenzyme, the AC activity of MdTTM1 is related to divalent cations in the reaction system, such as Mn2+ than Mg2+ and Ca2+. MdTTM1 shows a much higher AC activity with the support of Mn2+ than Mg2+ and Ca2+
additional information
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as metalloenzyme, the AC activity of MdTTM2 is related to divalent cations in the reaction system, such as Mn2+ than Mg2+ and Ca2+. MdTTM2 shows a higher AC activity with the support of Mn2+ than Mg2+ and Ca2+
additional information
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Mg2+ and Ca2+ are essential for sustaining bicarbonate-stimulated rtsAC activity, but do not induce a clear dose-response on sAC activity by themselves under the assay conditions
additional information
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K+ is not required for induction of exocytosis by 8-bromo-cAMP, cAMP, or forskolin, but extracellular K+ is required for sporozoite apical regulated exocytosis itself via K+ channels
additional information
-
K+ is not required for induction of exocytosis by 8-bromo-cAMP, cAMP, or forskolin, but extracellular K+ is required for sporozoite apical regulated exocytosis itself via K+ channels
additional information
-
K+ is not required for induction of exocytosis by 8-bromo-cAMP, cAMP, or forskolin, but extracellular K+ is required for sporozoite apical regulated exocytosis itself via K+ channels
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INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
(4-(6-amino-9H-purin-9-yl)cyclopent-2-en-1-yl)acetic acid
-
i.e. PMC-4, type 2 enzyme, 50% inhibition at 6.998 mM, type 3 enzyme, 50% inhibition at 0.117 mM, type 5 enzyme, 50% inhibition at 0.22 mM
1,2,3,4,5,6,7,8,13,13,14,14-dodecachloro-1,4,4a,4b,5,8,8a,12b-octahydro-11-sulfo-1,4:5,8-dimethanotriphenylene-10-carboxylic acid
the compound defines an AC inhibitor scaffold with high affinity for human soluble isozyme and less inhibitory effect on mammalian transmembrane isozymes
1alpha,9alpha-dihydroxy-labd-13(E)-ene-8a,15-diol
-
a derivative of each of the two stereoisomers of labd-13(E)-ene-8a,15-diol, overview
1alpha-hydroxy-labd-13(E)-ene-8a,15-diol
-
a derivative of each of the two stereoisomers of labd-13(E)-ene-8a,15-diol, overview
2'(3')-O-(N-methylanthraniloyl)-guanosine 5'-[gamma-thio-]triphosphate
-
inhibits AC5, reduces basal L-type Ca2+ currents as a function of time, significantly and almost completely diminishes the increase of L-type Ca2+ currents due to isoproterenol, basal and isoproterenol-stimulated inhibition of L-type Ca2+ currents is concentration-dependent
2',3'-O-isopropylidene adenosine
-
specifically inhibits ACA in intact cells, without affecting ACB or ACG
2'-d-(3')-O-(N-methylanthraniloyl)-GTP
-
determination of Ki values under various experimental conditions
2'-d3'-AMP
P-site inhibitor, uncompetitive. A complemented state of the enzyme is strongly stabilized by the presence of the inhibitor and diphosphate; P-site inhibitor, uncompetitive. A complemented state of the enzyme is strongly stabilized by the presence of the inhibitor and diphosphate
2'-O-(N-methylanthraniloyl)-3'-deoxy-GTP
-
determination of Ki values under various experimental conditions
2,3-dibromo-1-(4-(hydroxy(oxido)amino)phenyl)-3-(4-quinolinyl)-1-propanone
-
2-(1H-benzimidazol-2-ylthio) propanoic acid 2-[(5-bromo-2 hydroxyphenyl)methylene] hydrazide
-
KH7
-
2-(1H-benzo[d]imidazole-2-ylthio)-N'-(5-bromo-2-hydroxybenzylidene) propanehydrazide
-
0.07 mM used in assay conditions
2-(4-(6-amino-9H-purin-9-yl)cyclopent-2-en-1-yl)-N-hydroxyacetamide
-
i.e. PMC-3, type 2 enzyme, 50% inhibition at 3.76 mM, type 3 enzyme, 50% inhibition at 0.098 mM, type 5 enzyme, 50% inhibition at 0.076 mM
2-(6-amino-9H-purin-9-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol
-
i.e. Ara-Ade, type 2 enzyme, 50% inhibition at 7.202 mM, type 3 enzyme, 50% inhibition at 0.375 mM, type 5 enzyme, 50% inhibition at 0.0098mM
2-amino-7-(2-furyl)-7,8-dihydroquinazolin-5(6H)-one
-
i.e. RS-2 or NKY80, type 2 enzyme, 50% inhibition at 2.63 mM, type 3 enzyme, 50% inhibition at 0.2264 mM, type 5 enzyme, 50% inhibition at 0.015 mM
2-amino-7-(4-chlorophenyl)-7,8-dihydroquinazolin-5(6H)-one
-
i.e.RS-4, type 3 enzyme, 50% inhibition at 6.61 mM, type 5 enzyme, 50% inhibition at 1.988 mM
2-amino-7-(4-methoxyphenyl)-7,8-dihydroquinazolin-5(6H)-one
-
i.e. RS-1, type 2 enzyme, 50% inhibition at 2.64 mM, type 3 enzyme, 50% inhibition at 1.32 mM, type 5 enzyme, 50% inhibition at 1.95 mM
2-amino-7-phenyl-7,8-dihydroquinazolin-5(6H)-one
-
i.e. RS-3, type 2 enzyme, 50% inhibition at 6.31 mM, type 3 enzyme, 50% inhibition at 0.56 mM, type 5 enzyme, 50% inhibition at 0.21 mM
2-hydroxy-17beta-estradiol
-
specific sAC inhibitor, blocks CO2/HCO3- mediated cAMP production
2-hydroxyestrone
-
reversible inhibition of recombinant soluble enzyme in dose dependent manner, IC50 in low micromolar range
3,20-dioxopregn-4-en-21-yl 4-bromobenzenesulfonate
discriminates between soluble isozyme and transmembrane isozymes, and appears to simultaneously block the original binding pocket and a neighboring interaction site
3-(6-amino-9H-purin-9-yl)-N-hydroxycyclopentanecarboxamide
-
i.e. PMC-6, type 2 enzyme, 50% inhibition at 0.065 mM, type 3 enzyme, 50% inhibition at 0.011 mM, type 5 enzyme, 50% inhibition at 0.00032 mM
4,5,6,7-tetrachloro-3,3-bis(6-hydroxy[1,1'-biphenyl]-3-yl)-2-benzofuran-1(3H)-one
-
4-(6-amino-9H-purin-9-yl)-N-hydroxybutanamide
-
i.e. PMC-2, type 3 enzyme, 50% inhibition at 0.32 mM, type 5 enzyme, 50% inhibition at 0.13 mM
4-(6-amino-9H-purin-9-yl)-N-hydroxycyclopent-2-ene-1-carboxamide
-
i.e. PMC-5, type 2 enzyme, 50% inhibition at 6.02 mM, type 3 enzyme, 50% inhibition at 0.137 mM, type 5 enzyme, 50% inhibition at 0.046 mM
5-(6-amino-9H-purin-9-yl)-N-hydroxypentanamide
-
i.e. PMC-1, type 2 enzyme, 50% inhibition at 1.303 mM, type 3 enzyme, 50% inhibition at 0.154 mM, type 5 enzyme, 50% inhibition at 0.030 mM
5-(6-amino-9H-purin-9-yl)tetrahydrofuran-3-ol
-
i.e. 2'5'-dd-Ado, type 2 enzyme, 50% inhibition at 2.382 mM, type 3 enzyme, 50% inhibition at 0.253 mM, type 5 enzyme, 50% inhibition at 0.0016 mM
6-chloro-N4-cyclopropyl-N4-[(thiophen-3-yl)methyl]pyrimidine-2,4-diamine
-
LRE1
-
9-(tetrahydrofuran-2-yl)-9H-purin-6-amine
-
i.e. SQ22536, type 2 enzyme, 50% inhibition at 0.285 mM, type 3 enzyme, 50% inhibition at 0.101 mM, type 5 enzyme, 50% inhibition at 0.0022 mM
9-tetrahydro-2'-furyladenine
-
effective and specific inhibitor for ACA in cell lysates and intact cells
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
-
effective and specific inhibitor for ACG in cell lysates
bithionol
potent, isoform Adcy10-specific inhibitor, noncompetitive with respect to ATP
Ca2+/calmodulin
-
the Ca2+/calmodulin inhibition of isoform AC3 occurs at rather high concentrations (0.1 mM/0.0005 mM)
-
Caffeine
-
inhibits cAMP accumulation by ACB and ACG. None among ACA, ACB and ACG is a direct target for the inhibitory effects of caffeine
Carbachol
-
increases intracellular calcium, inhibits A2bR mediated increase in cAMP by 53%
carbamazepine
-
carbamazepine preferentially inhibits forskolin-stimulated isoforms AC5 and AC1 and all D1 agonist-stimulated adenylate cyclases, with isoforms AC5 and AC7 being the most sensitive. When compared to 1 or 3 mM Mg2+, 10 mM Mg2+ reduces lithium-induced AC5 inhibition by 70%. Carbamazepine competes for adenylate cylcase's catechol-estrogen site
cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine
-
inhibits ACA, ACB and ACG
delta opioid receptor agonist DPDPE
-
i..e. d-Pen2,d-Pen5 enkephalin, delta opioid receptor agonist, 0.001 mM significantly represses forskolin-stimulated adenylyl cyclase activity
-
delta opioid receptor agonist DT II
-
i.e.(d-Ala2)-deltorphin II, delta opioid receptor agonist, 0.001 mM significantly represses forskolin-stimulated adenylyl cyclase activity
-
Foscarnet
-
a diphosphate analogue, is able to inhibit adenylate cyclase activity in cardiac myocytes, but does not inhibit activity of recombinant murine isozyme ACVI in virus-infected myocytes
Galphai
-
inhibits Galphas-stimulated activities of ACVI, Gbetagamma does not alter the ability of Galphai to inhibit the activities of ACVI
GALPHAI protein
-
inhibits basal activity of isoform V, not the basal activity of isoform VI
-
Galphai2G203T
chronic treatment of HEK-293T cells reduces AC5 activity
-
Gi GTP-binding protein
-
inhibitory G-protein signaling acts presynaptically to regulate release, and, when paired with elevations in the concentration of cyclic GMP, converts a transient cyclic GMP-induced depression into a long-lasting decrease in release, overview
-
Hexachlorophene
potent, isoform Adcy10-specific inhibitor, noncompetitive with respect to ATP
L-(+)-2,3-butanediol
-
isoform AC7 activity is inhibited to about 50% with 100 mM L-(+)-2,3-butanediol
labd-13(E)-ene-8a,15-diol
-
isolated from the resin Ladano of the plant Cistus creticus subsp. creticus that grows in the island of Crete, Greece. Docking calculations of the two stereoisomers of the compound and derivatives to the enzyme at the forskolin binding site, overview
Li+
-
lithium preferentially inhibits adenylyl cyclase V and VII isoforms, moderately also isozyme AC-II, but does not inhibit Ca2+-activated isozymes AC-I and AC-VIII, it interferes with the transduction pathways mediated via isozymes AC-V and AC-IIV. The inhibitor effect is abolished for the superactivated isozyme, overview
lithium
-
lithium preferentially inhibits isoform AC5, lithium competes with Mg2+, which is essential for adenylate cyclase activity
MDL-12330A
-
the adenylate cyclase inhibitor depresses the response in GRNs to trehalose as well as sucrose in gustatory receptor neurons
nitrosocysteine
CSNO, a nitrosyl group donor, the nitrosylating stress affects the catalytic activity of isozyme AC6 activity, activity significantly decreases with CSNO treatment
-
NKY80
-
selective adenylyl cyclase-V inhibitor, completely blocks both 5,5'-dimethyl-1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetra-acetic acidstimulated cAMP formation and renin release
noradrenaline
-
adenylate cyclase is almost completely inhibited by 0.5 mM noradrenaline
O2
adenylyl cyclase isoform 6 is the only member of the adenylyl cyclase enzyme family to be inhibited by low oxygen levels. Only AC6 is inhibited by hypoxia and nitrosylation
opioid receptor agonist DAMGO
-
i.e. (d-Ala2,N-MePhe4,Gly5-ol)enkephalin, micro opioid receptor agonist, 0.001 mM significantly represses forskolin-stimulated adenylyl cyclase activity
-
PAPANANOATE
-
nitric oxide donor, completely abolishes A2bR mediated cAMP production
pertussis toxin
chronic treatment of HEK-293T cells reduces AC5 activity
-
Ric8a
i.e., resistance to inhibitors of cholinesterase 8 homolog A, AC5 interacts with Ric8a through directly interacting at its N-terminus, selectively suppresses AC5 activity, does not further suppress AC5s activity in the presence of somatostatin, effectively suppresses the forskolin-stimulated activity of AC5, but not that of AC6. Treating cells with pertussis toxin or expressing a dominant negative Galphai mutant abolishes the suppressive effect, markedly suppresses the activation of AC5 induced by isoprenaline of a Galphas coupled receptor in an isoform-specific manner, while the isoprenaline-evoked activity of AC6 is not affected
-
RNAi
-
AC5, AC6 and AC9 isoform-specific stealth RNAi, increases A2bR levels 12fold. AC5, AC6 and AC9 levels are inhibited by 60-80%. AC5 RNAi does not affect the levels of AC6 RNA and vice versa. cAMP production is inhibited in AC6 RNAi transfected cells but not in cells transfected with AC5 and AC9 RNAi, indicating that AC6 is associated with A2bR
-
S-nitroso-N-acetylpenicillamine
-
nitric oxide donor, inhibits A2bR mediated increase in cAMP by 64%
siRNA
-
selectively reduces heterologous expression of AC6 without impact on the expression of AC2, reduces forskolin-activated AC6 activity, whereby diminishing forskolin-induced arborization
-
sufentanil
-
a mu-opioid receptor agonist, inhibits the forskolin-activated enzyme, the combined treatment with sufentanil and nimodipine, an L-type Ca2+ channel blocker, increases mu-opioid-mediated inhibition of adenylyl cyclase and switched it to a predominantly PTX-resistant response, overview
vitamin D
-
decreases parathyroid-induced stimulation of AC6 and induces a phosphorylation of AC6 in a PKC-dependent manner
Yotiao
-
the A-kinase anchoring protein Yotiao or AKAP9 binds and regulates adenylyl cyclase in brain, it inhibits AC2 and AC3, but has no effect on AC1 or AC9, the N-terminus of isozyme AC2, AC2-NT, acts as a competitive inhibitor of Yotiao-AC2 interactions, recombinantly expressed Yotiao from HEK293 cells
-
2'(3')-O-(N-methylanthraniloyl)-GTP
-
catalytic heterodimer VC1-IIC2, incompletely defined structure 2'- or 3'-substituted nucleoside triphosphate
2'(3')-O-(N-methylanthraniloyl)-ITP
-
most potent inhibitor of heart adenylyl cyclase and recombinant AC5
2'(3')-O-(N-methylanthraniloyl)-ITP
-
highest potency on both cortical and medullary adenylyl cyclase in presence of Mn2+ as well as in presence of Mg2+
2',3'-bis[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
catalytic heterodimer VC1-IIC2
2',3'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
catalytic heterodimer VC1-IIC2, incompletely defined structure 2'- or 3'-substituted nucleoside triphosphate
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
most potent inhibitor for isoforms ACI and ACII
2',5'-dideoxy-3'-ATP
-
a P-site inhibitor, binds to the cytoplasmic domains, structure overview
2',5'-dideoxy-3'-ATP
a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview; a P-site inhibitor, binds to the cytoplasmic domains, structure overview
2',5'-dideoxyadenosine
-
inhibitor significantly inhibits heparin-induced capacitation of sperm cells
2',5'-dideoxyadenosine
-
inhibits ACA, ACB and ACG in cell lysates, but not in intact cells
2',5'-dideoxyadenosine
massive inhibition of cAMP formation with a combination of enzyme inhibitors 9-(tetrahydro-29-furyl)adenine and 2',5'-dideoxyadenosine; massive inhibition of cAMP formation with a combination of enzyme inhibitors 9-(tetrahydro-29-furyl)adenine and 2',5'-dideoxyadenosine
2',5'-dideoxyadenosine
-
inhibits forskolin induced tmAC stimulation at 0.15 mM
2-hydroxyestradiol
-
reversible inhibition of recombinant soluble enzyme in dose dependent manner, IC50 in low micromolar range, trans-membrane enzyme VII IC50 of about 2 microM
2-hydroxyestradiol
-
selective sAC inhibitor, inhibits the jelly induced acrosome reaction by 30% as well as the increase in cAMP levels by 42%
3'-AMP
-
type 2 enzyme, 50% inhibition at 0.263 mM, type 3 enzyme, 50% inhibition at 0.030 mM, type 5 enzyme, 50% inhibition at 0.015 mM
4-hydroxyestradiol
-
reversible inhibition of recombinant soluble enzyme in dose dependent manner, IC50 in low micromolar range
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
catalytic heterodimer VC1-IIC2
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
catalytic heterodimer VC1-IIC2
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
catalytic heterodimer VC1-IIC2
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
catalytic heterodimer VC1-IIC2
ATP
-
substrate inhibition at high concentrations, inhibition is relieved in the presence of HCO3-, no substrate inhibition in the presence of 50 mM HCO3-
BAPTA
-
inhibition of Ca2+-stimulated AC, buffers cytosolic Ca2+ and shifts activation in the hyperpolarizing direction, so that MDL 12330A has little or no further effect
Ca2+
at low concentrations; inhibition by low concentrations
Ca2+
-
AC5 and AC6 are inhibited by Ca2+ at both sub- and supra-micromolar concentration, Ca2+ inhibits the soluble adenylate cyclase core composed of the C1 domain of AC5 and the C2 domain of AC2, at micromolar concentration Ca2+ inhibition is non-exclusive with respect to diphosphate, but at 0.1 mM Ca2+ and above inhibition appears to be exclusive with respect to diphosphate
Ca2+
-
addition of Ca2+ to cells which have been depleted of intracellular Ca2+ markedly suppress cAMP synthesis by AC9
Ca2+
-
Ca2+ stimulates transmembrane isozymes AC1 and AC8 via calmodulin, and inhibits AC5 and AC6 directly
Ca2+
-
cortical adenylyl cyclase AC5 is sensitive to inhibition by Ca2+
Ca2+
-
bradykinin receptor-mediated increases in the release of intracellular calcium inhibits AC6 activity
Ca2+
-
at 0.1 mM and higher, the calcium cations inhibit the adenylyl cyclase activity
DAMGO
-
a mu-opioid receptor agonist, inhibits the forskolin-activated enzyme, the combined treatment with sufentanil and nimodipine, an L-type Ca2+ channel blocker, increases mu-opioid-mediated inhibition of adenylyl cyclase and switched it to a predominantly PTX-resistant response, overview
EGTA
-
freshly activated CyaA is inhibited by EGTA at low calmodulin concentrations
inhibitory G protein
-
both alpha and betagamma subunits, activated by GTP binding, can modulate activity of effectors in transduction signaling, including adenylyl cyclase. In depressed patients, the expression of stimulatory G protein is increased and of inhibitory G protein is decreased, which suggests greater stimulation of the cAMP pathway
-
inhibitory G protein
-
isozyme group III is comprised of Gialpha /Ca2+ -inhibited isozymes AC5 and AC6. G proteins interact with AC mainly through their switch II alpha-helices, which are conformational sensors for the alpha-activation state, mode of regulation, overview
-
inhibitory G protein
-
Galphai subunits contribute to the reduction of adenylyl cyclase activity after either forskolin or GalphaS activation
-
inhibitory G protein
AC1 activity is regulated by both Ca2+ and G proteins
-
inhibitory G protein
isozyme group III is comprised of Gialpha /Ca2+ -inhibited isozymes AC5 and AC6. G proteins interact with adenylate cyclase mainly through their switch II alpha-helices, which are conformational sensors for the alpha-activation state, mode of regulation, overview; isozyme group III is comprised of Gialpha /Ca2+-inhibited isozymes AC5 and AC6. G proteins interact with adenylate cyclase mainly through their switch II alpha-helices, which are conformational sensors for the alpha-activation state, mode of regulation, overview
-
MDL 12330A
-
inhibitor of AC1 activity, shifts activation in the hyperpolarizing direction. Buffering cytosolic Ca2+ with the Ca2+ chelator BAPTA shifts activation in the hyperpolarizing direction, so that MDL 12330A has little or no further effect
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
catalytic heterodimer VC1-IIC2
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
catalytic heterodimer VC1-IIC2
NO
-
NO functions either via an as yet unidentified regulator of adenylyl cyclase or the enzyme itself is the target of NO, inhibition is reversed by reducing agents
NO
-
inhibits forskolin- and Galphas-stimulated activity of recombinant AC5 and AC6, but neither AC1 nor AC2 in N18TG2 cells
SQ 22536
i.e. 9-(tetrahydro-29-furyl)adenine, massive inhibition of cAMP formation with a combination of enzyme inhibitors 9-(tetrahydro-29-furyl)adenine and 2',5'-dideoxyadenosine; i.e. 9-(tetrahydro-29-furyl)adenine, massive inhibition of cAMP formation with a combination of enzyme inhibitors 9-(tetrahydro-29-furyl)adenine and 2',5'-dideoxyadenosine
SQ 22536
-
adenylyl cyclase inhibitor, blocks both generation of cAMP and the release of renin, completely blocks 5,5'-dimethyl-1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetra-acetic acidstimulated renin release and cAMP content
SQ22536
-
the adenyly cyclase inhibitor increases senescent human diploid fibroblast proliferation by inhibition of adenosine monophosphate-activated protein kinase via reduction of AMPKalpha phosphorylation at Thr172 by inhibiting the LKB signaling, molecular mechanism, overview
tyrphostin A25
-
IC50 0.119mM, IC50 forskolin-stimulated adenylyl cyclase 1 mM, 37°C, pH 7.5
additional information
-
antibodies against ACT fail to block Bordetella pertussis attachment to human A549 cells
-
additional information
-
not inhibited by methylanthraniloyl-IMP and anthraniloyl-IMP
-
additional information
the ATP analogs ATP-Sp-alphaS and ATP-Rp-alphaS are potent inhibitors
-
additional information
-
the ATP analogs ATP-Sp-alphaS and ATP-Rp-alphaS are potent inhibitors
-
additional information
-
PleD is subject to tight feedback inhibition by the product c-diGMP
-
additional information
-
sensitization of cAMP response is attenuated by PKC and Raf1 inhibitors
-
additional information
-
2-amino-7-(furanyl)-7,8-dihydro-5(6H)-quinazolinone does not inhibit ACG and has only a partial inhibitory effect on ACA and ACB
-
additional information
inhibition of mutant catalytic domains by 2'(3')-O-(N-methylanthraniloyl)-modified nucleotides is reduced compared to the wild-type catalytic domain Cya2-446, overview
-
additional information
-
inhibition of mutant catalytic domains by 2'(3')-O-(N-methylanthraniloyl)-modified nucleotides is reduced compared to the wild-type catalytic domain Cya2-446, overview
-
additional information
-
acute activation of cannabinoid receptor 1 leads to inhibition of isoenzymes ACI, AC III, AC VI and AC VIII
-
additional information
-
G protein coupled receptor kinase 2 by sequestering Gbetagamma subunits in vivo decreases isoproterenol-elicited increase in cAMP accumulation in cells expressing ACVI. Pertussis toxin treatment does not alter the ability of G protein coupled receptor kinase 2 to attenuate isoproterenol-stimulated ACVI activity
-
additional information
-
PAM, a protein associated with Myc, inhibits AC1 activity in the picomolar to nanomolar range, is ineffective in regulating stimulated AC2 activity
-
additional information
-
Epstein Barr virus infection prevents activation of the cAMP/PKA pathway, overview
-
additional information
structure-based development of adenylyl cyclase inhibitors, compounds exploiting the catechol estrogen binding site can produce potent, isoform discriminating adenylyl cyclase inhibitors, inhibitory potency of compounds, overview
-
additional information
-
structure-based development of adenylyl cyclase inhibitors, compounds exploiting the catechol estrogen binding site can produce potent, isoform discriminating adenylyl cyclase inhibitors, inhibitory potency of compounds, overview
-
additional information
-
maximal inhibition of forskolin-stimulated adenylyl cyclase by buprenorphine and nalbuphine is increased in cells expressing regulator of G protein signaling RGS-insensitive Galphao CIGS, Galphai2 CIGS, or Galphai3 CIGS compared with their GalphaCI counterparts, but the RGS-insensitive mutation has little or no effect on the maximal inhibition by DAMGO and morphine
-
additional information
-
2',3'-O-(2,4,6-trinitrophenyl)-nucleotides (TNP-nucleotides) inhibit isoform ACI in the order of potency TNP-UTP=TNP-ATP>TNP-GTP=TNP-CTP>TNP-ADP>TNP-GDP>>>TNP-AMP. Specifically, the order of potency for isoform ACII is TNP-UTP >TNP-ATP=TNP-CTP >TNP-GTP >>TNP-ADP>TNP-GDP > TNP-AMP. Specifically, TNP-nucleotides inhibit isoform ACV in the order of potency: TNP-ATP>TNP-UTP>TNP-GTP=TNP-CTP>>TNP-ADP>TNP-GDP>TNP-AMP
-
additional information
presence of diphosphate does not have a significant effect on either cyclase activity or FRET; presence of diphosphate does not have a significant effect on either cyclase activity or FRET
-
additional information
presence of diphosphate does not have a significant effect on either cyclase activity or FRET; presence of diphosphate does not have a significant effect on either cyclase activity or FRET
-
additional information
forskolin-interacting amino acids are not involved in the hypoxic inhibition mechanism
-
additional information
the enzymatic activity of full-length AC9 is largely insensitive to heterotrimeric G proteins. The AC9 isoform-specific carboxyl-terminal (C2b) domain exerts a seemingly paradoxical autoinhibitory effect by occluding the active site in the presence of Gsalpha-GTP
-
additional information
AC9 is insensitive to Galphai inhibition, but although AC9 is not directly inhibited by Galphai/o, it can heterodimerize with Galphai/o-regulated isoforms, AC5 and AC6
-
additional information
structure-based development of adenylyl cyclase inhibitors, compounds exploiting the catechol estrogen binding site can produce potent, isoform discriminating adenylyl cyclase inhibitors, inhibitory potency of compounds, overview
-
additional information
-
inhibition studies of the purified catalytic subunits in the presence of forskolin
-
additional information
-
inhibition of NO, superoxide and or prostaglandin formation does not affect vasopressin-stimulated cAMP accumulation
-
additional information
-
foscarnet, a diphosphate analogue, is able to inhibit adenylate cyclase activity in uninfected rat cardiac myocytes, but does not inhibit recombinant AC activity in murine isozyme ACVI virus-infected myocytes
-
additional information
-
cyclic AMP levels in photoreceptor cells are highest in darkness and reduced by light exposure, dopamine D4 receptor activation promotes light adaptation and suppresses the light-sensitive pool of cyclic AMP in photoreceptor cells
-
additional information
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
-
isozyme AC8 is neither stimulated by Gs nor inhibited by Gi
-
additional information
isozyme AC8 is neither stimulated by Gs nor inhibited by Gi
-
additional information
-
inhibition of adenylyl cyclase, especially of isozyme ACVII, is involved in somatostatin anti-angiogenic actions
-
additional information
-
valproate does not affect any forskolin- or D1 receptor-stimulated adenylate cyclase
-
additional information
at 1 mM, D-galactose, D-mannose, L-arabinose, L-rhamnose, D-glucose, D-fructose, fructose 1,6-bisphosphate, glucose 6-phosphate, DL-threonine, L-isoleucine, L-valine, L-asparagine, L-histidine, L-aspartic acid, D-alanine, L-alanine, L-cysteine, L-leucine, glycine, sodium chloride, potassium chloride, sodium citrate, sodium acetate, sodium bicarbonate, NADH, glyoxylic acid, alpha-ketoglutarate, pyruvate and phosphoenolpyruvate do not significantly affect activity of the holoenzyme
-
additional information
-
at 1 mM, D-galactose, D-mannose, L-arabinose, L-rhamnose, D-glucose, D-fructose, fructose 1,6-bisphosphate, glucose 6-phosphate, DL-threonine, L-isoleucine, L-valine, L-asparagine, L-histidine, L-aspartic acid, D-alanine, L-alanine, L-cysteine, L-leucine, glycine, sodium chloride, potassium chloride, sodium citrate, sodium acetate, sodium bicarbonate, NADH, glyoxylic acid, alpha-ketoglutarate, pyruvate and phosphoenolpyruvate do not significantly affect activity of the holoenzyme
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
HAMP domain of Rv1319c inhibits adenylyl cyclase activity; no inhibition of Rv1625c by P-site ATP analogues; the first ca. 200 amino acid region of Rv1264 holoenzyme is auto-inhibitory
-
additional information
addition of one or two residues results in a slightly more inhibited phenotype. Addition of three residues results in only subtle changes, probably because the insertion of three residues is compatible with an extra-helical turn. In contrast, insertion of nine amino acids almost abolishes pH sensitivity
-
additional information
-
addition of one or two residues results in a slightly more inhibited phenotype. Addition of three residues results in only subtle changes, probably because the insertion of three residues is compatible with an extra-helical turn. In contrast, insertion of nine amino acids almost abolishes pH sensitivity
-
additional information
-
class I AC is unaffected by up to 0.03 mM poly-phosphate 75
-
additional information
-
the enzyme is insensitive to forskolin and 2,5-dideoxyadenosine (2,2-DDA), both modulators of transmembrane adenylyl cyclases
-
additional information
-
tyramine receptor activation with tyramine reduces adenylyl cyclase activity in a dose-dependent manner
-
additional information
-
full-length enzyme contains a large autoinhibitory C-terminal
-
additional information
-
Galpha0 is not sufficient to inhibit AC5 or AC6, inhibition requires an intact cell membrane or additional protein interactions that are absent in a reconstituted in vitro system
-
additional information
-
selective PKC inhibitor, abolishes cAMP accumulation by AC2
-
additional information
-
oxidative stress decreases the enzyme stimulation through GTPgammaS, GSalpha proteins, and hormones, overview
-
additional information
soluble adenylyl cyclase inhibitors reduce not only basal Isc, but also Isc stimulated by two distinct agonists, forskolin and aldosterone, suggesting that soluble adenylyl cyclase activity may be regulating electrogenic Na+ transport at a site common to all pathways, soluble adenylyl cyclase inhibition blocks ATPase activity without affecting surface expression of the Na+ pump
-
additional information
-
structure-based development of adenylyl cyclase inhibitors, compounds exploiting the catechol estrogen binding site can produce potent, isoform discriminating adenylyl cyclase inhibitors, overview
-
additional information
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
the soluble isozyme contains a C-terminal autoinhibitory domain that reduces Vmax without affecting the substrate affinity
-
additional information
-
monovalent ions exhibit dose-dependent inhibition from 30 to 200 mM
-
additional information
-
lipopolysaacharides differentially affect the soluble and transmembrane isozymes in nuclei and chloroplasts
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
1,2,3-propanetriol
-
isoform AC6 shows about 10% stimulation of activity with 100 mM 1,2,3-propanetriol, isoform AC7 shows about 18% stimulation of activity with 100 mM 1,2,3-propanetriol, isoform AC9 shows about 15% stimulation of activity with 100 mM 1,2,3-propanetriol
1,2-Butanediol
-
isoform AC6 shows about 37% stimulation of activity with 100 mM 1,2-butanediol, isoform AC7 shows about 38% stimulation of activity with 100 mM 1,2-butanediol, isoform AC9 shows about 32% stimulation of activity with 100 mM 1,2-butanediol
1,3-butanediol
-
isoforms AC6 and AC7 show about 22% stimulation of activity with 100 mM 1,3-butanediol, isoform AC9 shows about 17% stimulation of activity with 100 mM 1,3-butanediol
1,3-Propanediol
-
isoform AC6 shows about 17% stimulation of activity with 100 mM 1,3-propanediol, isoform AC7 shows about 20% stimulation of activity with 100 mM 1,3-propanediol, isoform AC9 shows about 17% stimulation of activity with 100 mM 1,3-propanediol
1,4-Butanediol
-
isoform AC6 shows about 30% stimulation of activity with 100 mM 1,4-butanediol, isoform AC7 shows about 25% stimulation of activity with 100 mM 1,4-butanediol, isoform AC9 shows about 40% stimulation of activity with 100 mM 1,4-butanediol
1-butanol
-
isoform AC6 shows about 85% stimulation of activity with 100 mM 1-butanol, isoform AC7 shows about 110% stimulation of activity with 100 mM 1-butanol, isoform AC9 shows about 105% stimulation of activity with 100 mM 1-butanol
1-propanol
-
isoform AC6 shows about 31% stimulation of activity with 100 mM 1-propanol, isoform AC7 shows about 50% stimulation of activity with 100 mM 1-propanol, isoform AC9 shows about 44% stimulation of activity with 100 mM 1-propanol
2,3-Butanediol
-
isoform AC6 shows about 30% stimulation of activity with 100 mM 2,3-butanediol, isoform AC7 shows about 35% stimulation of activity with 100 mM 2,3-butanediol, isoform AC9 shows about 41% stimulation of activity with 100 mM 2,3-butanediol
2-butanol
-
isoform AC6 shows about 60% stimulation of activity with 100 mM 2-butanol, isoform AC7 shows about 70% stimulation of activity with 100 mM 2-butanol, isoform AC9 shows about 60% stimulation of activity with 100 mM 2-butanol
2-propanol
-
isoform AC6 shows about 20% stimulation of activity with 100 mM 2-propanol, isoform AC7 shows about 35% stimulation of activity with 100 mM 2-propanol, isoform AC9 shows about 40% stimulation of activity with 100 mM 2-propanol
A-77636
-
a dopamine receptor agonist, the activation by can be reversed by D1-receptor antagonists SCH23390, SKF83566, and butaclamol
acetazolamide
-
when apical membrane insertion of the vacuolar proton pumping ATPase is stimulated by treatment with acetazolamide, sAC is also concentrated in the apical membrane of A-intercalated cells
AmOctbeta2R
-
an 2-adrenergic-like octopamine receptor activating adenylyl cyclase activity in the honeybee Apis mellifera. The monoaminergic receptor family in the homometabolic Apis mellifera is complex in holometabolic model insects, cf. Drosophila melanogaster. When heterologously expressed in an eukaryotic cell line, AmOctbeta2R causes a decrease in [cAMP]i. The receptor displays a pronounced preference for octopamine over tyramine, but does not react on serotonin and dopamine. The sequence of AmOctbeta2R contains several putative sites for posttranslational modification. Four potential N-glycosylation sites (N-X-(S/T)) are present in the extracellular N-terminus: N27MT, N164NT, N238GS, and N243ET. Conserved cysteine residues (C336 and C414) in the first and second extracellular loops might form a disulfide bridge as found in other biogenic amine receptors. Five consensus sites for phosphorylation by protein kinase C and one consensus site for phosphorylation by protein kinase A are found in the cytoplasmic domains of the receptor protein. Phylogenetic analysis and functional features, overview
-
BIM-1
-
specific protein-kinase C inhibitor, significantly increases cumulus cell cAMP concentrations
CAP
-
for full activation of the AC in vivo RAS2-GTP, CAP and Gpa2 modulate the enzyme synergistically
Carbachol
-
carbachol-induced capacitative Ca2+ entry clearly stimulates AC8-mediated cAMP production at the single-cell level
crude extract of cytosolic proteins from CHO cells
-
at least 500fold increased adenylate cyclase activity
-
D-(-)-2,3-butanediol
-
isoforms AC6 and AC7show about 30% stimulation of activity with 100 mM D-(-)-2,3-butanediol, isoform AC9 shows about 10% stimulation of activity with 100 mM D-(-)-2,3-butanediol
D-glucose
-
the stimulatory effect of D-glucose does not change in the presence of Ca2+ and calmodulin antagonists chloropromazine, N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride, and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride
dihydrexidine
-
a dopamine receptor agonist, the activation by can be reversed by D1-receptor antagonists SCH23390, SKF83566, and butaclamol
EGF
-
the stimulatory effect of EGF on adenylyl cyclase activity is enhanced in the presence of 0.005 mM Ca2+ and decreased in the presence of 0.1 mM Ca2+
-
G protein subunit
-
requirement for dual regulation of the AC by both Gs activation and Ca2+/calmodulin in a time-dependent manner
-
GALPHAS protein
-
250fold stimulation isoform V, 500fold stimulation isoform VI
-
Gbeta1gamma2
-
increases the activation of ACV and ACVI by forskolin or Galphas. Gbetagamma subunits derived from sources other than Gi participate in mediating the full activation of ACVI by the beta-adrenergic receptor agonist, isoproterenol
-
glucagon-like peptide-1
-
stimulates the enzyme via activation of the specific G protein-coupled receptor GLP-1
-
Gpa2
-
for full activation of the AC in vivo RAS2-GTP, CAP and Gpa2 modulate the enzyme synergistically
-
GSalpha proteins
-
mediate stimulation of the adenylyl cyclase in case of hyperglycemia
-
guanosine 5'-(beta,gamma-imido)tri-phosphate
-
up to 4fold stimulation
guanosine 5'-(gamma-thio)triphosphate
-
stimulation of enzyme activity up to 3.5fold
H89
-
specific inhibitor of protein-kinase A, significantly increases cumulus cell cAMP concentrations at 0.0001 and 0.03 mM
Insulin
-
the stimulatory effect of insulin on adenylyl cyclase is decreased to 28% in the presence of 0.1 mM Ca2+
-
ionomycin
-
increases intracellular Ca2+ concentrations, significantly increases cumulus cell cAMP concentrations
L-(+)-2,3-butanediol
-
isoform AC6 shows about 55% stimulation of activity with 100 mM L-(+)-2,3-butanediol, isoform AC9 shows about 45% stimulation of activity with 100 mM L-(+)-2,3-butanediol
meso-2,3-butanediol
-
isoform AC6 shows about 15% stimulation of activity with 100 mM meso-2,3-butanediol, isoform AC7 shows about 28% stimulation of activity with 100 mM meso-2,3-butanediol, isoform AC9 shows about 10% stimulation of activity with 100 mM meso-2,3-butanediol
NaCl
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1647 is slightly activated at 500 mM
Nicotine
-
nicotine treatment in adulthood produces an immediate increase in adenylate cyclase activity in males that disappears upon withdrawal, nicotine increases the activating effect of forskolin, especially in males, overview
PaOctbeta2R
-
an 2-adrenergic-like octopamine receptor activating adenylyl cyclase activity in the american cockroach Periplaneta americana. The monoaminergic receptor family in the hemimetabolic Periplaneta americana is similarly complex as in holometabolic model insects like Drosophila melanogaster and the honeybee, Apis mellifera. Phylogenetic analysis. The receptor is 100fold more selective for octopamine than for tyramine. The deduced amino acid sequence consists of 457 residues with a calculated molecular weight of 52.1 kDa and a pI of 8.73. The protein has 7 predicted transmembrane domains, structure and membrane topology, tissue distribution and expression pattern. overview
-
protein kinase A
-
stimulates cAMP in the brain, the activation is increased in brains of patients with bipolar mood disorders, overview
-
Protein kinase C
phosphorylation
-
staurosporine
-
non-specific protein-kinase C inhibitor, significantly increases cumulus cell cAMP concentrations
synthetic muramyl dipeptides
-
subunits of bacterial peptidoglycan, strong activation of the enzyme and of hyphal growth, NMR analysis, overview. The LRR domain of Cyr1p is required as bindin gsite for Candida albicans response to the peptides, overview. Synergistic effects of synthetic muramyl dipeptides and CO2
-
[8-arginine]vasopressin
-
0.01 mM [8-arginine]vasopressin significantly activates cortical and medulla adenylyl cyclase
-
5,5'-dimethyl-1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetra-acetic acid
-
cytosolic calcium chelator, reduces isolated juxtaglomerular intracellular calcium, allowing an increased activity of the calcium-inhibitable isoform adenylyl cyclase-V, stimulates both cAMP and renin release
5,5'-dimethyl-1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetra-acetic acid
-
decreases intracellular calcium, stimulates adenylyl cyclase, increases intracellular cAMP content by 125% and basal renin by 182%
A2B adenosine receptor
-
activates the enzyme and regulates its activity and the cAMP signaling pathway in mast and microvascular cell, role of the C-terminus of the A2B receptor in stimulation of adenylate cyclase, which is important for A2B receptor coupling to Gs-adenylate cyclase, overview
-
A2B adenosine receptor
-
activates the enzyme and regulates its activity and the cAMP signaling pathway in mast and microvascular cell, role of the C-terminus of the A2B receptor in stimulation of adenylate cyclase, which is important for A2B receptor coupling to Gs-adenylate cyclase, overview
-
alpha subunit of the guanine-nucleotide binding regulatory protein
-
activation
-
bicarbonate
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
stimulates purified Rv1319c catalytic domain
bicarbonate
-
HCO3-, stimulates the enzyme at physiologically relevant levels for fish internal fluids (about 7 mM)
Calmodulin
-
requirement for dual regulation of the AC by both Gs activation and Ca2+/calmodulin in a time-dependent manner
Calmodulin
activates, the N-terminal portion of CaM binds to the beta-hairpin region in the CA domain of CyaA, interaction mode, structure analysis of the calmodulin-CyaA complex and interface, and mechanism of catalytic activation, detailed overview. The N-terminus of CaM is linked to the C-terminus of CaM by a flexible linker with a defined degree of freedom. The potency of CaM D50C mutant to activate CyaA is enhanced about 10fold, mutants T26C or T41C
Calmodulin
-
the catalytic domain of CyaA corresponds to the first 370 residues of the toxin and binds with high affinity to calmodulin, CaM, a ubiquitous Ca2+-dependent regulator in eukaryotic cells. CaM binding triggers major structural re-arrangements in AC and stimulates its enzymatic activity more than a 1000fold to reach the highest catalytic turnovers known for AC enzymes with a kcat higher than 3000/s in optimal conditions. In the absence of CaM, AC still exhibits a residual activity of 1-3/s, which is on a par with many other AC enzymes
Calmodulin
-
mechanism of activation of adenylate cyclase by calmodulin (CaM), overview. Dependence of steady-state velocities on CaM and ATP concentrations suggests that CaM and ATP bind to the enzyme in a random fashion. A pre-steady-state lag phase is observed when adenylate cyclase is added to solutions of CaM and ATP, reflecting the association of AC and CaM. Analysis of pre-steady-state data indicates that CaM binds to AC and AC:ATP with second-order rate constants of 30 and 60 microM-1 s-1, respectively, and that CaM dissociates from the resultant complexes with a first-order rate constant of 0.002 s-1. A biphasic dependence of steady-state velocities on CaM concentration is observed: the first phase extending from 0.01 to 1 nM CaM (Kd,obs = 0.06 nM) and the second phase from 1 to 2000 nM CaM (Kd,obs = 60 nM). These results suggest that AC exists in at least two conformations, with each conformation exhibiting distinct binding affinity for CaM and distinct potential for activation
Calmodulin
a second isoform- and regulator-specific contact site in C2 is necessary to render enzyme activity susceptible to calmodulin modulation. In addition to the PFAHL-motif in C1b of ACII, calmodulin requires not only the Ca2+-independent AC28-region in C1b but also a Ca2+-dependent domain in C2a of ACI with the VLG-loop to stimulate this adenylyl cyclase isoform
Calmodulin
calmodulin activation of isoform Adcy1 can be regulated by selctive oxidation of the C-terminal Met residues in calmodulin, and by two N-terminal Met residues, M36 and M51. CaM with all Met residues oxidized is unable to activate the enzyme
Calmodulin
-
co-application of 200 nM Ca2+ and calmodulin enhances the rate of cAMP synthesis by a factor of about 2.5
Calmodulin
-
stimulates AC8 which shows a dis-inhibitory activation mechanism, Ca2+ stimulates transmembrane isozymes AC1 and AC8 via calmodulin, and inhibits AC5 and AC6 directly
Calmodulin
AC1 activity is regulated by both Ca2+/calmodulin and G proteins
cAMP
-
the stimulatory effect of cAMP on adenylyl cyclase activity is enhanced in the presence of 0.005 mM Ca2+ and decreased in the presence of 0.1 mM Ca2+
CO2
-
induces acidification of cells, accompanied by a rise in intracellular HCO3-
dopamine
-
140% activation at 0.1 mM, activation in hippocampus and striatum, the stimulation is partially inhibited, up to 48%, by oxotremorine, inhibition of stimulation is blocked by muscarinic toxin MT3, purified from Dendroaspis angusticeps snake venom, overview
dopamine
-
a dopamine receptor agonist, the activation by can be reversed by D1-receptor antagonists SCH23390, SKF83566, and butaclamol
Epidermal growth factor
-
stimulates AC5, which is required for activation of a KCa1.1 channel in vascular smooth muscle and the subsequent upregulation of genes critical for cell proliferation
Epidermal growth factor
-
increases cAMP accumulation in a GTP-dependent manner, enhances AC5 activity via phosphorylation of Galphas on one or more tyrosine residues
ethanol
AC7 is the most ethanol responsive isoform, N-terminal 28-amino-acid region of the C1a domain and the C-terminal region of the AC molecule are important for the enhancement of AC activity by ethanol
ethanol
AC3 is far less responsive, AC2 is less responsive to ethanol than human AC7, N-terminal 28-amino-acid region of the C1a domain and the C-terminal region of the adenylate cyclase molecule are important for the enhancement of adenylate cyclase activity by ethanol
ethanol
AC2 is less responsive to ethanol than rat AC3 or human AC7, N-terminal 28-amino-acid region of the C1a domain and the C-terminal region of the AC molecule are important for the enhancement of AC activity by ethanol
forskolin
-
stimulates the activity of soluble forms of ACV comprising their C1 and C2 domains, but Gbeta1gamma2 does not alter the ability of the agonist to regulate adenylate cyclase activity
forskolin
-
actions of Ca2+ chelator BAPTA are overcome by exposure to 0.001 mM forskolin, a direct stimulator of AC1, to restore cAMP levels
forskolin
-
free G protein Gsalpha subunits enhance adenylate cyclase responses to forskolin
forskolin
-
stimulates Gbetagamma subunits whereby enhancing the activity of enzymes
forskolin
-
leads to cAMP accumulation in C6 glioma cells expressing the mu-opioid-receptor
forskolin
-
free G protein Gsalpha subunits enhance adenylate cyclase responses to forskolin
forskolin
-
decreased forskolin-stimulated adenylyl cyclase activity in suicide subjects
forskolin
-
activated by 0.001 mM forskolin, coapplication of geldanamycin (0.1-10 nM) effectively suppresses the increase in forskolin-activated adenylate cyclase activation by 56%
forskolin
forskolin binds cyclase relatively weakly in the absence of the Galphas subunit. The presence of Galphas substantially increases the ability of forskolin to complement and activate the cyclase
forskolin
AC9 is forskolin-insensitive. But AC9-containing Sf9 membranes treated with forskolin in the presence of high concentrations of Galphas are weakly activated compared with membranes treated with Galphas alone
forskolin
FSK, residues T500, N503, and S1035 interact with forskolin, ligand docking analysis. Mutations of T500, N503, or S1035 decrease FSK-stimulated AC activity. FSK-interacting amino acids are not involved in the hypoxic inhibition mechanism. Elucidation of the FSK binding site in isozyme AC6
forskolin
-
binds to the cytoplasmic domains, structure overview. Isozyme group IV contains forskolin-insensitive isozyme AC9, mode of regulation, overview
forskolin
-
activates isozymes AC-I to AC-VIII, but not AC-IX, which contains no forskolin binding site
forskolin
binds to the cytoplasmic domains, structure overview. Isozyme group IV contains forskolin-insensitive isozyme AC9, mode of regulation, overview
forskolin
-
forskolin increases basal AC activity in Sf9 cell membranes expressing isoforms AC1 and AC2 by about 2-5fold, forskolin activates ACs in the order of potency AC1>AC5>mouse heart AC >AC2
forskolin
-
forskolin-stimulated cAMP production is significantly increased to levels that do not differ between isoforms following the expression of AC1, AC2, AC5, or AC6
forskolin
-
direct adenylate cyclase agonist, causes smaller increases in contraction and Ca2+ transient amplitudes in aged compared to younger ventricular myocytes
forskolin
-
activation in hippocampus, striatum, and amygdala. The stimulation is inhibited in vivo by oxotremorine, which is not affected by scopolamine. M4 is the main subtype responsible for muscarinic inhibition of forskolin-stimulated enzyme, overview
forskolin
-
activates the enzyme, the mu-opioid selective agonists sufentanil and DAMGO inhibit forskolin-stimulated adenylyl cyclase activity through a mechanism involving pertussis toxin sensitive Gai/o subunits, overview
forskolin
-
forskolin activation is elevated by nicotine treatment in adolescence, especially in males
forskolin
-
increases cAMP in both the plasma membrane and cytosolic compartments, induces inter-endothelial cell gaps in cells expressing the soluble adenylate cyclase, when the soluble chimaera is relocalized to the plasma membrane, the forskolin-stimulated adenylate cyclase activity does not induce gaps
G-protein
betagamma subunits
-
G-protein
activation by betagamma subunits
-
G-protein
betagamma subunit
-
Galphas
-
stimulates the activity of soluble forms of ACV comprising their C1 and C2 domains, but Gbeta1gamma2 does not alter the ability of the agonist to regulate adenylate cyclase activity
-
Galphas
-
stimulates Gbetagamma subunits whereby enhancing the activity of enzymes
-
Gbetagamma
a second isoform- and regulator-specific contact site in C2 is necessary to render enzyme activity susceptible to Gbetagamma modulation. In addition to the PFAHL-motif in C1b of ACII, Gbetagamma contacts the KF-loop in C2
-
Gbetagamma
-
Gbetagamma conditionally stimulates ACVI, but does not stimulate ACV
-
glucagon
-
0.04 mM glucagon significantly activates cortical and medulla adenylyl cyclase
Gsalpha
Q1MU16
signal transduction from beta-adrenergic receptors via trimeric Gs proteins to their downstream targets, e.g. ACs
-
GTPgammaS
-
in the presence of Mg2+, GTPgammaS increases adenylyl cyclase activity 4fold, with an EC50 value of 80 nM
GTPgammaS
-
stimulates the enzyme in hyperglycemic and control vascular smooth muscle cells
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
HCO3-
-
50 mM, 5-20fold activation in the presence of Mg2+, 3fold activation in the presence of Mn2+
HCO3-
-
50 mM, 5-20fold activation in the presence of Mg2+, 3fold activation in the presence of Mn2+
isoproterenol
-
isoproterenol-stimulated AC activity is potentiated by bile salts activation of PKCalpha and delta
isoproterenol
-
in the presence of GTP (0.01 mM), isoproterenol increases adenylyl cyclase activity approximately 2fold, with an EC50 value of 12 nM
isoproterenol
-
stimulates AC6 resulting in a significant increase in the arborization process
NKH 477
-
application of NKH 477, a water-soluble forskolin analog, stimulates membrane-bound adenylyl cyclase
NKH477
-
half-maximal activation with NKH477 is in the low micromolar range with 0.0102 mM for isoform AC3 and 0.0036-0.0081 mM for native enzyme
norepinephrine
Q1MU16
activates endogenously expressed b-adrenergic receptors, signal transduction from beta-adrenergic receptors via trimeric Gs proteins to their downstream targets, e.g. ACs
pertussis toxin
-
catalyses ADP-ribosylation of a cysteine residue on GalphaI, causing the G-protein complex to become uncoupled from the receptor, significantly increases cAMP concentrations
-
pituitary adenylate cyclase-activating polypeptide
-
i.e. PACAP, a neurotrophic and neuromodulatory peptide, differentially modulates AMPA receptor-mediated current in CA1 pyramidal neurons by activation of PAC1 and VPAC2 receptors, both involving the cAMP/PKA pathway, mechanism and regulation, overview. It also enhances NMDA receptor-mediated currents
-
Ras2
-
in its GTP-bound form is essential for activation in vivo and functions as a direct stimulator of adenylate cyclase activity in vitro
-
Ras2
-
for full activation of the AC in vivo RAS2-GTP, CAP and Gpa2 modulate the enzyme synergistically
-
serotonin
-
AC2 stimulation followed by cAMP accumulation, no effect on AC5. AC2 co-transfected with Gs protein shows a synergistic effect on both baseline and agonist-stimulated cAMP accumulation. In the combined presence of Golf and AC2, the level of cAMP accumulation is enhanced in the agonist-stimulated cell line to levels equaling those of the AC2-expressing cell line only, with no effect on baseline activity. Similarly, when AC5 is co-expressed with Gs a synergistic effect with this pairing on both baseline and agonist-stimulated cAMP accumulation versus control can be observed. Because baseline activity is so high with the AC5/Gs pairing, the difference between stimulated and non-stimulated treatments is not significant. The AC5/Golf pairing fails to show any enhancement in cAMP accumulation upon serotonin stimulation, and no effect on baseline activity
serotonin
-
the stimulatory effect of serotonin on adenylyl cyclase activity (253%) is enhanced in the presence of 0.005 mM Ca2+
stimulating G protein
-
both alpha and betagamma subunits, activated by GTP binding, can modulate activity of effectors in transduction signaling, including adenylyl cyclase. In depressed patients, the expression of stimulatory G protein is increased and of inhibitory G protein is decreased, which suggests greater stimulation of the cAMP pathway
-
stimulating G protein
GalphaS, and Gbeta1 and Ggamma2 subunits, G-protein-coupled receptors couple Galphas and activate isozyme ACVI
-
stimulating G protein
-
activating Gsalpha migrates from lipid rafts to nonraft membrane domains in prefrontal cortex and cerebellum in response to chronic, but not acute, treatment with tricyclic or selective serotonin reuptake inhibitor antidepressants, resulting in a more facile association with adenylyl cyclase and increased of cAMP formation. The alteration in membrane localization is unique to Gsalpha, another caveolae and lipid raft resident G-protein, Gqalpha is unaltered
-
stimulating G protein
-
i.e. s-Gs, comprising G protein subunits beta and gamma, binds to the cytoplasmic domains, structure overview, isozyme group II consists of Gbetagamma-stimulated AC 2, 4 and 7, G proteins interact with AC mainly through their switch II alpha-helices, which are conformational sensors for the alpha-activation state, mode of regulation, overview
-
stimulating G protein
i.e. s-Gs, comprising G protein subunits beta and gamma, binds to the cytoplasmic domains, structure overview, isozyme group II consists of Gbetagamma-stimulated AC 2, 4 and 7, G proteins interact with adenylate cyclase mainly through their switch II alpha-helices, which are conformational sensors for the alpha-activation state, mode of regulation, overview
-
stimulating G protein
AC1 activity is regulated by both Ca2+/calmodulin and G proteins
-
stimulating G protein
-
Galphai subunits contribute to the reduction of adenylyl cyclase activity after either forskolin or GalphaS activation
-
stimulating G protein
GalphaS proteins, the activation of the chimeric mutant dimer of AC2/AC5 is highly increased compared to the single isozymes, overview
-
thapsigargin
-
increases intracellular Ca2+ concentrations, significantly increases cumulus cell cAMP concentrations
thapsigargin
-
thapsigargin-induced capacitative Ca2+ entry clearly stimulates AC8-mediated cAMP production at the single-cell level
additional information
-
is activated by different host cell factors and is inactive until injected into the host cell
-
additional information
-
is activated by different host cell factors and is inactive until injected into the host cell
-
additional information
-
cholera toxin, KN-62, phorbol-12-myristate-13-acetate and BAPTA-am or a combination of 3 mM EGTA plus BAPTA-am have no effect on cAMP concentrations
-
additional information
-
the transmembrane isozyme is induced by light, overview
-
additional information
-
the upstream regulator of Cyr1p, RAS1, is required for optimal response of the organism to synthetic muramyl dipeptides
-
additional information
-
delta-opoid receptor activation sensitizes subsequent stimulation of AC6 signaling and enhances AC6 phosphorylation
-
additional information
-
cytosolic regulator of AC essential for activation of ACA, ACG is activated by high osmolarity
-
additional information
-
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
insensitive to either Ca2+ or betagamma subunits of G-proteins
-
additional information
-
acute activation of cannabinoid receptor 1 leads to stimulation of isoenzymes AC II, AC IV and AC VII
-
additional information
-
adenylyl cyclase isoenzyme IX is not activated by forskolin
-
additional information
-
prior activation of AC8 is not strictly necessary to observe Ca2+-driven cAMP dynamics. Nevertheless, amplitude of the transients is enhanced when AC8 is stimulated
-
additional information
-
phosphorylation of a C-terminally located threonine residue increases activity of AC2 in intact HEK-293 cells
-
additional information
-
binding of agonists to receptors leads to the activation of G proteins, which in turn activate adenylyl cyclase, overview
-
additional information
no stimulation by sphingosine 1-phosphate in HEK 293 cells but synergistic effect on isoproterenol activation, overview
-
additional information
no stimulation by sphingosine 1-phosphate in HEK 293 cells but synergistic effect on isoproterenol activation, overview
-
additional information
-
isoforms AC6, AC7 and AC9 are not significantly stimulated by 1,2,4-butanetriol and 1,2,3,4-butanetetraol
-
additional information
design of a selective activator of adenylyl cyclase 6 based on the forskolin structure
-
additional information
the enzymatic activity of full-length AC9 is largely insensitive to heterotrimeric G proteins. No isoproterenol-induced cAMP response attributable to wild-type AC9 is reliably
-
additional information
-
2-4fold enhancement of adenylate cyclase activity by the histidine kinase-receiver system, histidine kinase domain autophosphorylates on His572, subsequently the phosphate is transferred to the second receiver domain Asp895, which is adjacent to the CHD domain
-
additional information
-
no activation of the soluble isozyme by GTP, guanosine 5'(betagamma-imido)-triphosphate, forskolin, fluorde, and cholera toxin. The transmembrane isozyme is induced by light, overview
-
additional information
-
in hypoxia isozyme ACVII expression is enhanced in wild-type retinas and it is further increased in sst2-lacking retinas, whereas in sst2 overexpressing retinas the increase of ACVII is lower than in wild-type retinas, overview
-
additional information
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
-
isozyme AC8 is neither stimulated by Gs nor inhibited by Gi
-
additional information
isozyme AC8 is neither stimulated by Gs nor inhibited by Gi
-
additional information
-
no activation by histamine, glucagon, neuropeptide Y, and serotonin
-
additional information
not stimulated by calcium, bicarbonate and forskolin
-
additional information
-
not stimulated by calcium, bicarbonate and forskolin
-
additional information
regulatory domain of Rv1264 regulates AC activity in a pH-dependent manner, activated at acidic pH due to pH-dependent structural transitions of the Rv1264 dimer, strongly activated by the addition of fatty acids, oleic acid may serve as a hinge
-
additional information
-
regulatory domain of Rv1264 regulates AC activity in a pH-dependent manner, activated at acidic pH due to pH-dependent structural transitions of the Rv1264 dimer, strongly activated by the addition of fatty acids, oleic acid may serve as a hinge
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
HAMP domain of Rv3645 activates adenylyl cyclase activity
-
additional information
unsaturated fatty acids strongly stimulate Rv2212 activity by increasing substrate affinity, greatly enhance the pH sensitivity, thus converting Rv2212 to a pH sensor adenylyl cyclasemore. At 1 mM, D-galactose, D-mannose, L-arabinose, L-rhamnose, D-glucose, D-fructose, fructose 1,6-bisphosphate, glucose 6-phosphate, DL-threonine, L-isoleucine, L-valine, L-asparagine, L-histidine, L-aspartic acid, D-alanine, L-alanine, L-cysteine, L-leucine, glycine, sodium chloride, potassium chloride, sodium citrate, sodium acetate, sodium bicarbonate, NADH, glyoxylic acid, alpha-ketoglutarate, pyruvate and phosphoenolpyruvate do not significantly affect activity of the holoenzyme
-
additional information
-
unsaturated fatty acids strongly stimulate Rv2212 activity by increasing substrate affinity, greatly enhance the pH sensitivity, thus converting Rv2212 to a pH sensor adenylyl cyclasemore. At 1 mM, D-galactose, D-mannose, L-arabinose, L-rhamnose, D-glucose, D-fructose, fructose 1,6-bisphosphate, glucose 6-phosphate, DL-threonine, L-isoleucine, L-valine, L-asparagine, L-histidine, L-aspartic acid, D-alanine, L-alanine, L-cysteine, L-leucine, glycine, sodium chloride, potassium chloride, sodium citrate, sodium acetate, sodium bicarbonate, NADH, glyoxylic acid, alpha-ketoglutarate, pyruvate and phosphoenolpyruvate do not significantly affect activity of the holoenzyme
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
activity of Rv1264 is be regulated by pH
-
additional information
-
the transmembrane isozyme is induced by light, overview
-
additional information
Q7A2D9
GAF domains bind cAMP and thereby increase the adenylate cyclase activity 27fold, thus functioning as an autoactivating switch and creating a feed-forward stimulatory mechanism
-
additional information
Q8YVS0
GAF domains bind cAMP and thereby increase the adenylate cyclase activity 27fold, thus functioning as an autoactivating switch and creating a feed-forward stimulatory mechanism
-
additional information
Q8YMH0
GAF domains bind cAMP and thereby increase the adenylate cyclase activity 27fold, thus functioning as an autoactivating switch and creating a feed-forward stimulatory mechanism
-
additional information
-
is activated by different host cell factors and is inactive until injected into the host cell
-
additional information
completely insensitiv to forskolin and GTPgammaS
-
additional information
-
prolonged depolorization of cells, in the absence of Ca2+ leads to an increase in cAMP accumulation
-
additional information
the soluble isozyme is insensitive to the regulation by forskolin and G proteins, but seems to be activated by a proteolytic mechanism
-
additional information
-
chronic treatment with mu-opioid agonists leads to upregulation of the of the cAMP-signalling pathway
-
additional information
-
no activation of the soluble isozyme by the transmembrane isozyme-specific activator forskolin
-
additional information
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
-
measurement of dopamine receptor agonist activation in a competitive assay with antagonists, e.g. SCH23390, overview
-
additional information
-
two signals activate the single, class IIId AC in vivo, a shift from carbohydrate-free to glucose-containing medium and an intracellular acidification upon carbon starvation
-
additional information
-
the transmembrane isozyme is induced by light, overview, lipopolysaacharides differentially affect the soluble and transmembrane isozymes in nuclei and chloroplasts
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
KM VALUE [mM]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.004
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 2 mM Mn2+ and 0.1 mM cAMP
0.005
ATP
Q7CH76
mutant enzyme C83A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.011
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 2 mM Mn2+
0.011
ATP
Q7CH76
mutant enzyme R63A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.013
ATP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.014
ATP
Q7CH76
mutant enzyme D55K, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.015
ATP
Q7CH76
mutant enzyme E12Q, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.02
ATP
Q7CH76
wild type enzyme, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.024
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 10 mM Mg2+ and 0.1 mM cAMP
0.027
ATP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.03
ATP
Q7CH76
mutant enzyme F5A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.035
ATP
Q7CH76
mutant enzyme L72A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.035
ATP
Q7CH76
mutant enzyme M140A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.038
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 10 mM Mg2+
0.046
ATP
Q7CH76
mutant enzyme K76A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.05
ATP
recombinant adenylyl cclase, in the presence of Mn2+
0.05
ATP
Q7CH76
mutant enzyme R113A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.06
ATP
Q7CH76
mutant enzyme E136A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.086
ATP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.09
ATP
Q7CH76
mutant enzyme K14A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.094
ATP
-
after activation of soluble AC with the stimulatory G protein alpha protein and GTP-gamma-S in the presence of Mn2+
0.1
ATP
-
Sf9, Mn2+, pH 7.4, 37°C, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.1
ATP
Q7CH76
mutant enzyme E10Q, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.12
ATP
recombinant AC expressed from synthetic AC gene PfAC526-884
0.13
ATP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.153
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant Y394A, 10 mM Mg2+
0.16
ATP
Q7CH76
mutant enzyme E136A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.165
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant W374A, 10 mM Mg2+
0.168
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant W249A, 10 mM Mg2+
0.201
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant K136A, 10 mM Mg2+
0.21
ATP
Q7CH76
mutant enzyme K14A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.216
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant E242A, 10 mM Mg2+
0.24
ATP
Q7CH76
mutant enzyme E10Q, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.259
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant K253A, 10 mM Mg2+
0.275
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant E185A, 10 mM Mg2+
0.284
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant K260A, 10 mM Mg2+
0.327
ATP
-
25°C, plasma membrane isolated from glutamate/malate grown cells
0.33
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant S113A, 10 mM Mg2+
0.398
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant T189A, 10 mM Mg2+
0.4
ATP
Q7CH76
mutant enzyme K76A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.43
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mn2+, 0.1 mM forskolin, stimulatory G protein alpha subunits guanosine 5'-(gamma-thio)triphosphate
0.46
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant R19A, 10 mM Mg2+
0.533
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant S106A, 10 mM Mg2+
0.55
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mn2+, stimulatory G protein ALPHA subunits guanosine 5'-(gamma-thio)triphosphate
0.56
ATP
-
after activation of soluble AC with the stimulatory G protein alpha protein and GTP-gamma-S in the presence of Mg2+
0.6
ATP
-
recombinant C-terminal cytoplasmic domain of type II adenylyl cyclase
0.62
ATP
Q7CH76
mutant enzyme C83A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.682
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant K332A, 10 mM Mg2+
0.75
ATP
Q7CH76
mutant enzyme R63A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.76
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mg2+, stimulatory G protein alpha subunits guanosine 5'-(gamma-thio)triphosphate
0.78
ATP
Q7CH76
wild type enzyme, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.85
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mg2+, 0.1 mM forskolin, stimulatory G protein alpha subunits guanosine 5'-(gamma-thio)triphosphate
0.87
ATP
Q7CH76
mutant enzyme D55K, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
1.15
ATP
Q7CH76
mutant enzyme E12Q, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
1.19
ATP
Q7CH76
mutant enzyme M140A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
1.89
ATP
Q7CH76
mutant enzyme F5A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
2.29
ATP
Q7CH76
mutant enzyme L72A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
3.5
ATP
recombinant adenylyl cclase, in the presence of Mg2+
4.7
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant S103A, 10 mM Mg2+
additional information
additional information
apparent Km for MnATP 0.393 mM
-
additional information
additional information
-
apparent Km for MnATP 0.393 mM
-
additional information
additional information
-
Km value for Mn2+-ATP is higher in the presence of inorganic carbon than Cl-
-
additional information
additional information
steady-state FRET experiments of wild-type and mutant enzyme and calmodulin, overview
-
additional information
additional information
-
steady-state FRET experiments of wild-type and mutant enzyme and calmodulin, overview
-
additional information
additional information
Arrhenius plots, Michaelis-Menten kinetic model
-
additional information
additional information
Arrhenius plots, Michaelis-Menten kinetic model
-
additional information
additional information
Michaelis-Menten kinetics
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
TURNOVER NUMBER [1/s]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
1
ATP
-
pH and temperature not specified in the publication, in absence of calmodulin
8.8
ATP
-
after activation of soluble AC with the stimulatory G protein alpha protein and GTP-gamma-S in the presence of Mn2+
15.5
ATP
-
after activation of soluble AC with the stimulatory G protein alpha protein and GTP-gamma-S in the presence of Mg2+
2000 - 3000
ATP
-
pH and temperature not specified in the publication, in presence of calmodulin
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
kcat/KM VALUE [1/mMs-1]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
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Ki VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.00028
2',3'-O-bis(5-acetamidoanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.000091
2',3'-O-bis(5-bromoanthraniloyl)-ADP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0000126
2',3'-O-bis(5-bromoanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00002
2',3'-O-bis(5-bromoanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.000016
2',3'-O-bis(5-chloroanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.000015
2',3'-O-bis(5-chloroanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0065
2',3'-O-bis(5-methylanthraniloyl)-ADP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00036
2',3'-O-bis(5-methylanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0025
2',3'-O-bis(5-methylanthraniloyl)-CTP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0066
2',3'-O-bis(5-methylanthraniloyl)-IDP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.02
2',3'-O-bis(5-methylanthraniloyl)-IMP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.003
2',3'-O-bis(5-methylanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0007
2',3'-O-bis(5-propylanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0021
2',3'-O-bis(5-propylanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.012
2',3'-O-bis-anthraniloyl-IMP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00071
3'-O-(5-acetamidoanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0048
3'-O-(5-acetamidoanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0087
3'-O-(5-bromoanthraniloyl)-ADP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00033
3'-O-(5-bromoanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00092
3'-O-(5-bromoanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00035
3'-O-(5-chloroanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0007
3'-O-(5-chloroanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.00082
3'-O-(5-propylanthraniloyl)-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0038
3'-O-(5-propylanthraniloyl)-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.0075
bis-acetamido-anthraniloyl-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
additional information
additional information
-
inhibition of forskolin-stimulated adenylyl cyclase by mu-opioid recptor agonists in cells expressing different forms of G proteins, overview
-
0.000011
2'(3')-O-(N-methylanthraniloyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000011
2'(3')-O-(N-methylanthraniloyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000061
2'(3')-O-(N-methylanthraniloyl)-ATP
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.00011
2'(3')-O-(N-methylanthraniloyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.00011
2'(3')-O-(N-methylanthraniloyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.000125
2'(3')-O-(N-methylanthraniloyl)-ATP
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.001628
2'(3')-O-(N-methylanthraniloyl)-ATP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.003558
2'(3')-O-(N-methylanthraniloyl)-ATP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.05
2'(3')-O-(N-methylanthraniloyl)-ATP
pH 8.0, 37°C, versus ATP, wild-type catalytic domain Cya2-446
0.00006
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000075
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000706
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000872
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000051
2'(3')-O-(N-methylanthraniloyl)-CTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000072
2'(3')-O-(N-methylanthraniloyl)-CTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.003115
2'(3')-O-(N-methylanthraniloyl)-CTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.004141
2'(3')-O-(N-methylanthraniloyl)-CTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000013
2'(3')-O-(N-methylanthraniloyl)-GTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000014
2'(3')-O-(N-methylanthraniloyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000014
2'(3')-O-(N-methylanthraniloyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000032
2'(3')-O-(N-methylanthraniloyl)-GTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.00013
2'(3')-O-(N-methylanthraniloyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.00013
2'(3')-O-(N-methylanthraniloyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.001087
2'(3')-O-(N-methylanthraniloyl)-GTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.001249
2'(3')-O-(N-methylanthraniloyl)-GTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000027
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000042
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000468
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000666
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000006
2'(3')-O-(N-methylanthraniloyl)-ITP
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000009
2'(3')-O-(N-methylanthraniloyl)-ITP
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000029
2'(3')-O-(N-methylanthraniloyl)-ITP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.00003
2'(3')-O-(N-methylanthraniloyl)-ITP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.00001
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000014
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000047
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.00005
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.000022
2'(3')-O-(N-methylanthraniloyl)-UTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.000031
2'(3')-O-(N-methylanthraniloyl)-UTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mn2+, at 30°C, pH not specified in the publication
0.001435
2'(3')-O-(N-methylanthraniloyl)-UTP
-
medulla adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.0015
2'(3')-O-(N-methylanthraniloyl)-UTP
-
cortical adenylyl cyclase, in the presence of 7 mM Mg2+, at 30°C, pH not specified in the publication
0.0055
2',3'-bis[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0055
2',3'-bis[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0067
2',3'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.0067
2',3'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.00014
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.00037
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0011
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0013
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.0013
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.002
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.002
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0048
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0048
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0074
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.017
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.017
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.021
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.021
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0000037
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000009
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000081
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000081
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000099
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0001
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0001
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.000024
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000031
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.00011
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.00011
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.00011
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.00031
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.00031
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.00041
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0012
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0034
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.0081
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0081
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0094
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.0094
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000023
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000027
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000083
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000083
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.00022
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.00043
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.00043
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.0000071
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
isoform ACI, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000015
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
isoform ACV, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000024
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
isoform ACII, in 10 mM MnCl2, 100 mM KCl, 25 mM HEPES/NaOH, pH 7.4, at 30°C
0.000092
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.000092
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000092
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.000092
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.00064
2',3'-O-(N-anthraniloyl)-ADP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00086
2',3'-O-(N-anthraniloyl)-ADP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0029
2',3'-O-(N-anthraniloyl)-ADP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00012
2',3'-O-(N-anthraniloyl)-ATP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00013
2',3'-O-(N-anthraniloyl)-ATP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00064
2',3'-O-(N-anthraniloyl)-ATP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0043
2',3'-O-(N-anthraniloyl)-IMP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0074
2',3'-O-(N-anthraniloyl)-IMP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0075
2',3'-O-(N-anthraniloyl)-IMP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00079
2',3'-O-(N-methylanthraniloyl)-ADP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0013
2',3'-O-(N-methylanthraniloyl)-ADP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0029
2',3'-O-(N-methylanthraniloyl)-ADP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0001
2',3'-O-(N-methylanthraniloyl)-ATP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00015
2',3'-O-(N-methylanthraniloyl)-ATP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00033
2',3'-O-(N-methylanthraniloyl)-ATP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00058
2',3'-O-(N-methylanthraniloyl)-CDP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00074
2',3'-O-(N-methylanthraniloyl)-CDP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0037
2',3'-O-(N-methylanthraniloyl)-CDP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00015
2',3'-O-(N-methylanthraniloyl)-CTP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00015
2',3'-O-(N-methylanthraniloyl)-CTP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00069
2',3'-O-(N-methylanthraniloyl)-CTP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000053
2',3'-O-(N-methylanthraniloyl)-GTP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00009
2',3'-O-(N-methylanthraniloyl)-GTP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00061
2',3'-O-(N-methylanthraniloyl)-GTP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000034
2',3'-O-(N-methylanthraniloyl)-GTPgammaS
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000063
2',3'-O-(N-methylanthraniloyl)-GTPgammaS
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00037
2',3'-O-(N-methylanthraniloyl)-GTPgammaS
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000031
2',3'-O-(N-methylanthraniloyl)-IDP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000039
2',3'-O-(N-methylanthraniloyl)-IDP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000086
2',3'-O-(N-methylanthraniloyl)-IDP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0044
2',3'-O-(N-methylanthraniloyl)-IMP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0068
2',3'-O-(N-methylanthraniloyl)-IMP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0085
2',3'-O-(N-methylanthraniloyl)-IMP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0000012
2',3'-O-(N-methylanthraniloyl)-ITP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0000028
2',3'-O-(N-methylanthraniloyl)-ITP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000014
2',3'-O-(N-methylanthraniloyl)-ITP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000032
2',3'-O-(N-methylanthraniloyl)-ITPgammaS
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00004
2',3'-O-(N-methylanthraniloyl)-ITPgammaS
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00012
2',3'-O-(N-methylanthraniloyl)-ITPgammaS
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00034
2',3'-O-(N-methylanthraniloyl)-UDP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00039
2',3'-O-(N-methylanthraniloyl)-UDP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0027
2',3'-O-(N-methylanthraniloyl)-UDP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000032
2',3'-O-(N-methylanthraniloyl)-UTP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000046
2',3'-O-(N-methylanthraniloyl)-UTP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00046
2',3'-O-(N-methylanthraniloyl)-UTP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0011
2',3'-O-(N-methylanthraniloyl)-XTP
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0013
2',3'-O-(N-methylanthraniloyl)-XTP
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.003
2',3'-O-(N-methylanthraniloyl)-XTP
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00032
2'-deoxy-3'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00036
2'-deoxy-3'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0048
2'-deoxy-3'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00027
2'-deoxy-3'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00041
2'-deoxy-3'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0013
2'-deoxy-3'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.000065
3'-deoxy-2'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00047
3'-deoxy-2'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.00054
3'-deoxy-2'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0018
3'-deoxy-2'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC1, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0018
3'-deoxy-2'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC5, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0087
3'-deoxy-2'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
isoform AC2, in 75 mM Tris/HCl, pH 7.4, at 37°C
0.0094
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.0094
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.01
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.01
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.058
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.058
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.1
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.1
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.000001
9-[2-(phosphonomethoxy)ethyl]adenine diphosphate
-
in the presence of Mn2+
0.000025
9-[2-(phosphonomethoxy)ethyl]adenine diphosphate
-
in the presence of Mg2+
0.033
cytidine 5'-(gamma-thio)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.071
cytidine 5'-(gamma-thio)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
1
GTP
-
in 50 mM Tris-HCl (pH 8.0), 50 mM NaCl, 10 mM MgCl2, 10 mM CaCl2, at 37°C
2.4
guanosine 5'-(beta,gamma-imido)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
3
guanosine 5'-(beta,gamma-imido)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.4
guanosine 5'-(gamma-thio)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.41
guanosine 5'-(gamma-thio)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.35
inosine 5'-(beta,gamma-imido)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.48
inosine 5'-(beta,gamma-imido)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.02
inosine 5'-(gamma-thio)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.021
inosine 5'-(gamma-thio)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.0094
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.0094
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin and GTPgammaS-activated Galphas
0.011
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
0.011
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
VC1-IIC2 in the presence of 0.1 mM forskolin
2.5
uridine 5'-(beta,gamma-imido)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
2.8
uridine 5'-(beta,gamma-imido)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.015
uridine 5'-(gamma-thio)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.051
uridine 5'-(gamma-thio)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
10
xanthosine 5'-(beta,gamma-imido)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
10
xanthosine 5'-(beta,gamma-imido)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.02
xanthosine 5'-(gamma-thio)triphosphate
-
S49 cyc-, Mn2+, 100 microM forskolin
0.025
xanthosine 5'-(gamma-thio)triphosphate
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
IC50 VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.005
1,2,3,4,5,6,7,8,13,13,14,14-dodecachloro-1,4,4a,4b,5,8,8a,12b-octahydro-11-sulfo-1,4:5,8-dimethanotriphenylene-10-carboxylic acid
Limnospira platensis
-
0.00073
2',5'-dideoxy-3'-adenosine triphosphate
Mycobacterium avium
IC50 of about 730 nM
0.1
2,3-dibromo-1-(4-(hydroxy(oxido)amino)phenyl)-3-(4-quinolinyl)-1-propanone
Limnospira platensis
about
0.005
2-(1H-benzimidazol-2-ylthio) propanoic acid 2-[(5-bromo-2 hydroxyphenyl)methylene] hydrazide
Oncorhynchus mykiss
-
pH 7.4, temperature not specified in the publication
-
0.043
4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid
Homo sapiens
-
in 50 mM Tris-HCl (pH 8.0), 50 mM NaCl, 10 mM MgCl2, 10 mM CaCl2, at 37°C
0.1
4,5,6,7-tetrachloro-3,3-bis(6-hydroxy[1,1'-biphenyl]-3-yl)-2-benzofuran-1(3H)-one
Limnospira platensis
about
0.07
5'-benzyl-12'-hydroxy-2'-methyl-3',6',18-trioxoergotaman
Limnospira platensis
about
0.018
6-chloro-N4-cyclopropyl-N4-[(thiophen-3-yl)methyl]pyrimidine-2,4-diamine
Oncorhynchus mykiss
-
pH 7.4, temperature not specified in the publication
-
0.000033
cyclic poly-phosphate 17
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.002
cyclic triphosphate
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.00021
diphosphate
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
11
phosphate
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.0001
poly-phosphate 16
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.000027
poly-phosphate 25
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.000018
poly-phosphate 30
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
-
0.000012
poly-phosphate 45, poly-phosphate 68
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
-
0.000011
poly-phosphate 75
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
-
0.00002
Triphosphate
Mycobacterium tuberculosis
-
recombinant enzyme, in 50 mM Tris-HCl (pH 7.5), at 30°C
0.03
2',3'-O-isopropylidene adenosine
Dictyostelium discoideum
-
inhibition of DcAMP-induced ACA activation in intact cells
0.031
2',3'-O-isopropylidene adenosine
Dictyostelium discoideum
-
inhibition of ACA in intact cells
2.18
2',3'-O-isopropylidene adenosine
Dictyostelium discoideum
-
inhibition of ACA in cell lysates
0.00578
2-amino-7-(furanyl)-7,8-dihydro-5(6H)-quinazolinone
Dictyostelium discoideum
-
inhibition of ACB in cell lysates
1.31
2-amino-7-(furanyl)-7,8-dihydro-5(6H)-quinazolinone
Dictyostelium discoideum
-
inhibition of ACA in cell lysates
0.002
2-hydroxyestradiol
Homo sapiens
-
reversible inhibition of recombinant soluble enzyme in dose dependent manner, IC50 in low micromolar range, trans-membrane enzyme VII IC50 of about 2 microM
0.274
9-tetrahydro-2'-furyladenine
Dictyostelium discoideum
-
inhibition of ACA in cell lysates
0.812
9-tetrahydro-2'-furyladenine
Dictyostelium discoideum
-
inhibition of ACA in intact cells
0.016
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
Dictyostelium discoideum
-
inhibition of ACG in cell lysates
0.0166
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
Dictyostelium discoideum
-
inhibition of ACG in cell lysates
0.602
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
Dictyostelium discoideum
-
inhibition of ACG in intact cells
11.19
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
Dictyostelium discoideum
-
inhibition of ACA in intact cells
13.36
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
Dictyostelium discoideum
-
inhibition of ACB in intact cells
0.329
cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine
Dictyostelium discoideum
-
inhibition of ACA in cell lysates
0.497
cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine
Dictyostelium discoideum
-
inhibition of ACB in cell lysates
0.885
cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine
Dictyostelium discoideum
-
inhibition of ACG in cell lysates
0.119
tyrphostin A25
Homo sapiens
-
IC50 0.119mM, IC50 forskolin-stimulated adenylyl cyclase 1 mM, 37°C, pH 7.5
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
SPECIFIC ACTIVITY [µmol/min/mg]
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
0.00036
in the presence of 1 mM Mg2+, recombinant C-terminal CyaG domain
0.011
in the presence of 1 mM Mn2+, recombinant C-terminal CyaG domain
0.04
recombinant AC expressed from synthetic AC gene PfAC526-884
0.48
additional information
0.48
in the presence of physiological ATP concentrations and 1 mM Mn2+
additional information
-
Vmax forward reaction 1200/s, pH 7.2, 30°C, 0.1 microM free Ca2+, 147/s pH 7.2, 30°C, 2 microM free Ca2+
additional information
-
Vmax reverse reaction 2000/s, pH 7.2, 30°C, 0.1 microM free Ca2+, 100-300/s pH 7.2, 30°C, 2 microM free Ca2+
additional information
the specific activity of the catalytic domain fragment Cya2-446 and of the holoenzyme is independent of the protein concentration
additional information
-
the specific activity of the catalytic domain fragment Cya2-446 and of the holoenzyme is independent of the protein concentration
additional information
-
basal activity 5.6 pmol cAMP /10 min /mg protein, pH7.4, 22°C, 5mM Mg2+
additional information
-
soluble isozyme sAC activity from Sacytm1Lex/Sacytm1Lex brains, somatic sAC activity in brain is lower than activity in testis, overview
additional information
-
native Cya1, Vmax 65.7 pmol cAMP/min/nmol protein, pH 7.5, 27°C, Vmax 40.5 pmol cAMP/min/nmol protein, pH 7.5, 27°C, 50 mM NaHCO3
additional information
-
truncated Cya1, Vmax 17.6 pmol cAMP/min/nmol protein, pH 7.5, 27°C, Vmax 10.4 pmol cAMP/min/nmol protein, pH 7.5, 27°C, 50 mM NaHCO3
additional information
-
Vmax 66.3 pmol cAMP/min/nmol, ph 7.5, 27°C
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
10
5.8
6.8 - 7.4
7 - 8
7 - 9
7.4
7.5
8.5
9 - 9.5
9.5
additional information
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
additional information
Rv1647 has its pH optimum in the alkaline pH range
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pH RANGE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
5.3 - 8
-
approx. 20% of maximal activity at pH 5.3, approx. 50% of maximal activity at pH 8.0, recombinant CyaB1-maltose binding protein fusion
5.5 - 8
6 - 8
upon a shift from pH 8 to 6, Rv1264 is activated 40fold, pH sensitivity is linked to the N-terminal domain
6.5 - 9
holoenzyme has a 5fold higher activity at pH 6.5 compared to activity at pH 9, and with the catalytic domain the maximal activity difference in activity is 3fold between pH 6.5 and 7.6
7 - 9
8 - 8.6
additional information
5.5 - 8
isolated catalytic domain Rv1264 211-397, uniformly high enzyme activity
5.5 - 8
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
the Rv1264 holoenzyme shows higher adenylyl cyclase activity at pH 6.0. In contrast, the purified cyclase domain shows similar activities at both pH 5.5 and pH 8.0, pH sensing is not a property of any single amino acid in Rv1264 but a property of a network of interactions between the N-terminal and cyclase domains
additional information
-
ciliary beat frequency is stimulated by cAMP independently of intracellular pH
additional information
-
crystal forms of the native and His tagged enzyme appear to require pH below 5
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TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
20
30
37
40
45
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TEMPERATURE RANGE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
35 - 47
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ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
-
UniProt
brenda
several forms of the soluble isozyme, and a transmembrane isozyme
-
-
brenda
a self-fertile filamentous ascomycete, several strains, overview, gene sac1
UniProt
brenda
-
34754, 34755, 34756, 34757, 34758, 34759, 34798, 34803, 34810, 34811, 34812, 34819, 651177, 652269, 679129, 679879, 682024, 682829, 692600
-
-
brenda
-
34773, 34781, 34784, 34794, 34822, 34824, 649332, 651929, 652379, 653280, 653862, 664044, 665620, 665652
-
-
brenda
-
678381, 679107, 679659, 679862, 680828, 681009, 681169, 682112, 682285, 682958, 691237, 691562, 691711
-
-
brenda
-
693757, 693772, 694258, 694376, 695074, 695078, 707396, 707490, 708403, 709018, 709679, 709693, 710590, 713708, 729172, 730831
-
-
brenda
-
-
-
brenda
adult male C57BL6 mice and B1 vacuolar proton pumping ATPase deficient mice
-
-
brenda
-
UniProt
brenda
-
UniProt
brenda
maximal PfACalpha mRNA expression in the sexual stage
SwissProt
brenda
-
34769, 34774, 34775, 34779, 34785, 34792, 34800, 34807, 34808, 34809, 34816, 34820, 34821, 652157, 653132
-
-
brenda
-
679129, 679659, 680828, 681587, 681976, 682016, 682285, 682829, 691561, 693180, 693436, 693560, 693763
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-
brenda
-
-
-
brenda
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SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
-
glomeruli of the antennal lobes are specifically stained, whereas the core of the antennal lobes displays only weak labeling
brenda
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AC1 preferentially expressed in sino-atrial node cells, present as mRNA and as protein, AC5 present, AC8 absent
brenda
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forskolin-insensitive AC isoforms in various B cell populations
brenda
epithelial cells, both intercalated cells and principal cells
brenda
erythroleukemia cell line, high expression of isozyme AC7
brenda
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the insulin-secreting cells, derived from in vivo immortalized insulin-secreting pancreatic beta cells, are endogenously expressing Ca2+-sensitive AC isoforms
brenda
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isoform AC3 is evenly distributed in different sensory, central and motor neuropils
brenda
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pheromone detection in male mice depends on signaling through AC3
brenda
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isoform AC5 is the major adenylyl cyclase isoform in the cortex of the kidney
brenda
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in all intercalated cells, sAC and vacuolar proton pumping ATPase show considerable overlap under basal conditions, but sAC is also found in other cellular locations in the absence of vacuolar proton pumping ATPase. In type A-intercalated cells, both sAC and vacuolar proton pumping ATPase are apically and subapically located, whereas in type B-intercalated cells, significant basolateral colocalization of sAC and the vacuolar proton pumping ATPase is seen
brenda
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specific localization of the 50 kDa isoform to the axoneme of ciliated airway epithelial cells
brenda
additional information
isozyme AC8
brenda
isozyme AC6
brenda
isozyme AC5
brenda
isozyme AC1
brenda
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post-mortem Brodmanns area 9 and cerebellum from the right hemisphere from normal controls and suicide subjects, demographic characteristics, overview
brenda
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limbic system, induced and uninduced enzyme activity in different structures, overview
brenda
-
isozymes AC8, AC6, AC1, AC3, and AC2, high expression level of isozyme AC8 in numerous brain regions, including the hippocampus, thalamus, habenula, cerebellar cortex and hypothalamic supraoptic and paraventricular nuclei
brenda
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dorsal striatum and nucleus accumbens show a high content of isozyme AC5
brenda
isozyme AC1 is abundantly expressed within limbic regions of the central nervous system
brenda
isozyme AC5 is abundantly expressed within limbic regions of the central nervous system
brenda
isozyme AC8 is abundantly expressed within limbic regions of the central nervous system
brenda
isozyme AC8, high expression level of isozyme AC8 in numerous brain regions, including the hippocampus, thalamus, habenula, cerebellar cortex and hypothalamic supraoptic and paraventricular nuclei
brenda
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limbic system, induced and uninduced enzyme activity in different structures, overview
brenda
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highest AC1 expression, present in molecular layer, weak AC8 expression at postnatal day 7 and decreases further by postnatal day 14
brenda
-
highest AC1 expression, present in molecular layer, weak AC8 expression at postnatal day 7 and decreases further by postnatal day 14
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brenda
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ACIII localizes to cilia in adults, throughout the cortex, including the subiculum, as well as the retrosplenial granular, visual, motor, and orbital cortices
brenda
neonatal cardiac, isozyme AC2 is localized to the same structures in adult mice
brenda
neonatal cardiac, isozyme AC5 is localized to the same structures in adult mice
brenda
-
ACIII localizes to cilia in adults, throughout nuclei of the deep forebrain, including the nucleus accumbens, caudate/putamen, thalamus, and hypothalamus
brenda
-
synaptosome fractions from the adult brain show robust expression of AC1 in the postsynaptic density and extrasynaptic regions, while expression of AC8 is observed in the presynaptic active zone and extrasynaptic fractions
brenda
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synaptosome fractions from the adult brain show robust expression of AC1 in the postsynaptic density and extrasynaptic regions, while expression of AC8 is observed in the presynaptic active zone and extrasynaptic fractions
-
brenda
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expression of isozyme adenylyl cyclase VI, ACVI, at the left ventricular
brenda
isozyme AC2 is localized to the same structures in adult mice
brenda
isozyme AC5 is localized to the same structures in adult mice
brenda
-
isoforms AC3, AC5, and AC7 are detected in heart, AC5 is an important adenylyl cyclase isoform in heart
brenda
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high activity in sinoatrial nodal cells, and less in ventricular myocytes
brenda
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HEK-hD1, HEK-293 cells transiently transfected with human D1 dopamine receptor
brenda
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strong expression of AC1 in the dentate gyrus and CA2 regions, AC8 expression is restricted to the CA1 region
brenda
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lowest expression of AC1, protein increases in abundance in the neonatal hippocampus from postnatal days 714. By adulthood, abundant AC1 protein expression in the mossy fiber tract. AC8 protein levels are abundant during development, with diffuse and increasing expression in the hippocampus that intensify in the CA1/CA2 region by adulthood
brenda
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lowest expression of AC1, protein increases in abundance in the neonatal hippocampus from postnatal days 714. By adulthood, abundant AC1 protein expression in the mossy fiber tract. AC8 protein levels are abundant during development, with diffuse and increasing expression in the hippocampus that intensify in the CA1/CA2 region by adulthood
-
brenda
ventricular, isozyme AC2 is localized to the same structures in adult mice
brenda
ventricular, isozyme AC5 is localized to the same structures in adult mice
brenda
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ventricular, significantly less cAMP formation in response to adenylate cyclase stimulation in aged compared to younger cells
brenda
anterior cingulate cortex, ACC, neurons from a key region involved in high brain cognitive and executive functions
brenda
spinal commissural neuron cultures from embryonic day 14 from pregnant Sprague-Dawley rats
brenda
isozyme AC8, epithelium
brenda
isozyme AC3, epithelium
brenda
isozyme AC8
brenda
isozyme AC3
brenda
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cyclic AMP levels in photoreceptor cells are highest in darkness and reduced by light exposure
brenda
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cyclic AMP levels in photoreceptor cells are highest in darkness and reduced by light exposure
-
brenda
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localization of isozyme ACVII in photoreceptorouter segments, the outer plexiform layer, the inner plexiform layer and the ganglion cell layer
brenda
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AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina
brenda
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AC1 is a major adenylyl cyclase isoform controlling cyclic AMP synthesis in the mouse retina
-
brenda
isozyme AC6
brenda
isozyme AC2
brenda
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both tmAC and sAC present, presence of more than one tmAC isoform in sea urchin sperm
brenda
isozyme AC5
brenda
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isozymes AC8, AC6, AC5 and AC3, and a short 50 kDa splice variant sAC
brenda
isozyme AC8, and a short 50 kDa splice variant sAC
brenda
additional information
-
AC isoforms 1, 3, 4, 6, and 9 in cumulus cells. AC1, AC4 and AC6 predominate
brenda
additional information
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AC5 present and AC1 and AC8 absent in ventricular muscle, AC8 absent from cerebellum
brenda
additional information
-
AC1 and AC8 present at the apical pool of airway epithelial cells, specifically in ciliated cells, AC3 mainly present on the basolateral aspect
brenda
additional information
adenylyl cyclase 9 (AC9) is widely distributed in the body
brenda
additional information
-
ubiquitous expression of isozymes AC9, AC7 and AC4, and of a short 50 kDa splice variant sAC
brenda
additional information
-
predominance if not the exclusive presence of AC-V isoform in juxtaglomerular cells, AC-VI isoform not detectable
brenda
additional information
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primarily expresses AC3 mRNA in the inner medullary collecting duct, AC5 and AC6 also present
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
ubiquitous expression of isozymes AC9 and AC4
brenda
additional information
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ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
ubiquitous expression of a short 50 kDa splice variant sAC
brenda
additional information
-
predominance if not the exclusive presence of AC-V isoform in juxtaglomerular cells, AC-VI isoform not detectable
-
brenda
additional information
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AtT20 cell and secretory granules, AC9 present
-
brenda
additional information
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C6 glioma cell primarly expresses AC6, cardiomycete, in cardiac fibroblast AC6 present, in striatal neurons AC5 and AC6 present
brenda
additional information
-
tissue specific expression of cytosolic isozymes, overview
brenda
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LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
the soluble isozyme is attached to the cytoskeleton via protein-protein interactions
brenda
additional information
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
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brenda
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AC-V isoform dispersed throughout the cytoplasm in granule like foci, similar cytoplasmic localization for both renin and AC-V
brenda
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either/or both adenylyl cyclase types V and VI, colocalization of renin and adenylyl cyclase V/VI primarily on the granules
brenda
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AC-V isoform dispersed throughout the cytoplasm in granule like foci, similar cytoplasmic localization for both renin and AC-V
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brenda
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either/or both adenylyl cyclase types V and VI, colocalization of renin and adenylyl cyclase V/VI primarily on the granules
-
brenda
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the periplasmic moiety is linked to the T25 or T18 fragments by a transmembrane segment so that the cyclase fragments can remain in the cytosol
brenda
-
brenda
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
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brenda
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displays a clear voltage-sensor pore loop in tandem with a cytosolic AC homology domain
brenda
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displays a clear voltage-sensor pore loop in tandem with a cytosolic AC homology domain
brenda
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cytosolic AC activity overwhelms the barrier-protective effects of transmembrane AC activity in the formation of endothelial cells gaps
brenda
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displays a clear voltage-sensor pore loop in tandem with a cytosolic AC homology domain
brenda
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CyaA is synthesized as an inactive precursor proCyaA that is converted into an active toxin upon selective acylation of two lysine residues, K860 and K983, a modification that is carried out by a dedicated acyltransferase, CyaC. The acylated CyaA polypeptide is then secreted across the bacterial envelope by a specifc type I secretion machinery (T1SS) made of three components encoded by the cyaB, cyaD, and cyaE genes, which form an operon with the cyaA gene
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brenda
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outer membrane of cell with catalytic domain accessible on the outer surface
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the N-terminus is positioned intracellularly
brenda
-
brenda
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lipid rafts and cavaeolae, the localization mechanism involves the C-terminal C1 and C2 domains, which target the enzyme to the microdomains of the cells, localization of the structural features of C1 and C2 required for interaction with lipid rafts, overview
brenda
AC6 is a membrane-bound AC isoform (mAC). All mACs share architectural resemblance based on their protein sequences. They are membrane proteins with two membrane-bound regions, each with six transmembrane (TM) domains and two helices that link TM6 and TM12 to pseudo-symmetric cytosolic catalytic domains 1 (C1) and 2 (C2) with N- and C-terminals. Both terminal portions are highly variable, whereas the catalytic domains are mostly conserved
brenda
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nine transmembrane AC isozymes, of which four are sensitive to Ca2+
brenda
transmembrane enzyme
brenda
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6 transmembrane helices and a single cytosolic catalytic domain, which dimerizes to form a 12-transmembrane homodimeric enzyme
brenda
six putative helical transmembrane domains
brenda
in Rv3645 a membrane anchor consisting of 6 putative transmembrane helices is linked to a class IIIb CHD via a HAMP domain, the membrane anchor of Rv3645 may serve as a sensor
brenda
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
-
brenda
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c is a six-transmembrane protein with a single class III cyclase domain
brenda
-
six putative helical transmembrane domains
-
brenda
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in Rv3645 a membrane anchor consisting of 6 putative transmembrane helices is linked to a class IIIb CHD via a HAMP domain, the membrane anchor of Rv3645 may serve as a sensor
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brenda
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Rv1625c is a six-transmembrane protein with a single class III cyclase domain
-
brenda
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the N-terminal half of the class IIIb AC consists of a predicted membrane-associated sensor domain
brenda
transmembrane AC isozymes, some of which are sensitive to Ca2+
brenda
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present in the head, acrosomal and mitochondrial area and in flagellar membranes of sperm
brenda
soluble isozyme, only in its shortened, active form
brenda
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isolated from glutamate/malate or lactic acid grown cells
brenda
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sAC and the vacuolar proton pumping ATPase colocalize on or close to the apical plasma membrane in B1 vacuolar proton pumping ATPase deficient mice, colocalization does not require the B1 isoform
brenda
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AC8 is confined to lipid raft microdomains of the plasma membrane. AC8, Orai1 and STIM1 are co-localized in lipid raft domains of the plasma membrane
brenda
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membrane lipid microdomains of cardiac sinoatrial nodal pacemaker cells, the AC isozyme activity likely varies locally among membrane microdomains in correlation with their regulation mechanism, overview
brenda
AC8 is confined to lipid raft microdomains of the plasma membrane. AC8, Orai1 and STIM1 are co-localized in lipid raft domains of the plasma membrane
brenda
isozyme AC8 is preferentially localized in the presynaptic active zone and copurifies with Rab3A
brenda
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isozyme AC8 is preferentially localized in the presynaptic active zone and copurifies with Rab3A
-
brenda
additional information
a Kyte-Doolittle hydropathy plot of the LRR domain suggests several possible membrane-associated helices
-
brenda
additional information
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in SH-SY5Y cells AC9 mainly in irregular discrete punctae which are distinct from lysosomes, early endosomes or tubulovesicular endosomes
-
brenda
additional information
-
in AtT20 cells AC9 mainly in irregular discrete punctae which are distinct from lysosomes, early endosomes or tubulovesicular endosomes, AC9 present in the cis-Golgi network
-
brenda
additional information
-
close apposition between the enzyme and CCE channels
-
brenda
additional information
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in AtT20 cells AC9 mainly in irregular discrete punctae which are distinct from lysosomes, early endosomes or tubulovesicular endosomes, AC9 present in the cis-Golgi network
-
-
brenda
additional information
-
some of the longer rtsAC isoforms may be preferentially localized in the nucleus, the Golgi apparatus and podosomes
-
brenda
additional information
the soluble isozyme is bound to various compartments and structures in animals, e.g. mitochondria, centrioles, mitotic spindle, middle plate, and nucleus
-
brenda
additional information
close apposition between the enzyme and CCE channels
-
brenda
additional information
-
the enzyme occurs in almost all organelles of potato cells
-
brenda
Highest Expressing Human Cell Lines
Cell Line LinksPlease wait a moment until the data is sorted. This message will disappear when the data is sorted.
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
evolution
malfunction
physiological function
additional information
evolution
-
CyaA is a member of a large family of bacterial cytolysins known as RTX (repeat-in-toxin) toxins
evolution
-
Mycobacterium tuberculosis encodes for a rich cAMP machinery, consisting of 16 putative adenylyl cyclases, 10 proteins that harbor cyclic nucleotide-binding domains, and a single characterized phosphodiesterase. The presence of multiple genes encoding for adenylyl cyclases is correlated with the ability of this organism to synthesize and secrete elevated amounts of cAMP, providing a mechanism for the pathogen to hijack signaling within the macrophage. This family of adenylyl cyclase enzymes is found only in slow-growing mycobacteria. Sequence comparisons of adenylyl cyclases from Mycobacterium tuberculosis and Mycobacterium canetti
evolution
all plant taxonomic groups reproducing via motile sperm possess CAPE protein (with class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain), whereas those that do not produce motile sperm do not possess CAPE protein, with one exception in gymnosperm Cupressales. The phylogenic distribution of CAPE almost corresponds to the evolutionary history of motile sperm production
evolution
the AC family is composed of nine membrane-bound isoforms (AC1-AC9) and one soluble isoform
evolution
all plant taxonomic groups reproducing via motile sperm possess CAPE protein (with class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain), whereas those that do not produce motile sperm do not possess CAPE protein, with one exception in gymnosperm Cupressales. The phylogenic distribution of CAPE almost corresponds to the evolutionary history of motile sperm production
evolution
all plant taxonomic groups reproducing via motile sperm possess CAPE protein (with class III adenylyl cyclase (AC) in the C-terminal domain and class I phosphodiesterase (PDE) in the N-terminal domain), whereas those that do not produce motile sperm do not possess CAPE protein, with one exception in gymnosperm Cupressales. The phylogenic distribution of CAPE almost corresponds to the evolutionary history of motile sperm production
evolution
the enzyme is a Class IV AC enzyme, phylogenetic analysis
evolution
-
Mycobacterium tuberculosis encodes for a rich cAMP machinery, consisting of 16 putative adenylyl cyclases, 10 proteins that harbor cyclic nucleotide-binding domains, and a single characterized phosphodiesterase. The presence of multiple genes encoding for adenylyl cyclases is correlated with the ability of this organism to synthesize and secrete elevated amounts of cAMP, providing a mechanism for the pathogen to hijack signaling within the macrophage. This family of adenylyl cyclase enzymes is found only in slow-growing mycobacteria. Sequence comparisons of adenylyl cyclases from Mycobacterium tuberculosis and Mycobacterium canetti
-
evolution
-
Mycobacterium tuberculosis encodes for a rich cAMP machinery, consisting of 16 putative adenylyl cyclases, 10 proteins that harbor cyclic nucleotide-binding domains, and a single characterized phosphodiesterase. The presence of multiple genes encoding for adenylyl cyclases is correlated with the ability of this organism to synthesize and secrete elevated amounts of cAMP, providing a mechanism for the pathogen to hijack signaling within the macrophage. This family of adenylyl cyclase enzymes is found only in slow-growing mycobacteria. Sequence comparisons of adenylyl cyclases from Mycobacterium tuberculosis and Mycobacterium canetti
-
malfunction
-
inhibition of adenylyl cyclase in amygdala blocks the effect of audiogenic seizure kindling in genetically epilepsy-prone rats
malfunction
-
knockdown of AC5 and AC6 with siRNA reduces the ability of UDP to decrease cAMP
malfunction
-
glucose utilization is inhibited in adenylate cyclase deletion mutant CgYA in the presence of acetate
malfunction
the interface with GbetagammaC5 residues that are subject to gain-of-function mutations in humans with familial dyskinesia, indicating that the observed interaction is important for motor function. Many SNPs involve residues located near the Gbetagamma binding interface. Among them, R418W, A726T, M1029K, and DELTA9bp are associated with familial dyskinesia and represent gain-of-function mutations
malfunction
knockdown or knockout of endogenous AC9 reduces basal AC activity splenocytes
physiological function
-
adenylate cyclase plays an essential role in the acetate metabolism of Corynebacterium glutamicum
physiological function
-
the Chp chemotaxis-like system regulates intracellular cAMP levels by modulating CyaB activity
physiological function
-
cardiac-directed adenylyl cyclase 6 expression attenuates left ventricular hypertrophy and dysfunction in cardiomyopathy. Left ventricular contractility is increased, diastolic function is improved and left ventricular dilation is reduced by activation of adenylyl cyclase 6 expression
physiological function
-
transmembrane adenylyl cyclase regulates amphibian sperm motility through protein kinase A activation
physiological function
-
isoform AC3 is a likely candidate to fulfill an integrative role in sensory, motor and higher-order information processing in the honeybee brain
physiological function
-
the enzyme is involved in the activation of L-type Ca2+ channels in a HCO3--dependent braking pathway that results in elevated intracellular Ca2+ and activation of BK channels
physiological function
-
the Ca2+/calmodulin-dependent enzyme serves as a link between the inositol 1,4,5-trisphosphate/Ca2+ and the cAMP/protein kinase A signalling pathways in the salivary gland of the blowfly and is important for the amplification and optimization of the secretory response
physiological function
the enzyme is a key regulator of Pseudomonas aeruginosa virulence
physiological function
-
adenylyl cyclase activity is required in early-mid erythrocytic stages and functions as the parasite's pH sensor during growth inside red blood cells
physiological function
in primary cultures of dentate granule cells transfected with PAC, short-term elevation of intracellular cAMP levels induces axonal branching but not elongation, whereas long-term cAMP elevation induces both axonal branching and elongation. The temporal dynamics of intracellular cAMP levels regulate axonal branching and elongation through the activation of protein kinase A (PKA) and exchange protein directly activated by cAMP, respectively
physiological function
in transgenic myocytes overexpressing the enzyme, the sarcoplasmic reticulum Ca2+ content, fractional Ca2+ release, and twitch Ca2+ transient are significantly higher than in wild-type myocytes. Action potential duration is significantly longer in transgenic cells than in wild-type. Overexpressing myocytes developed spontaneous Ca2+ waves in a larger fraction compared with wild-type, particularly when cells were exposed to isoproterenol. Overexpressing hearts have increased levels of SERCA2a, oxidized Ca2+/calmodulin-dependent protein kinase II, and phosphorylation of ryanodine receptors at the CaMKII site, especially after isoproterenol treatment
physiological function
-
hyaluronic acid and heparin are physiological glycosaminoglycans capable of inducing in vitro capacitation in cryopreserved bull sperm, stimulating different enzymatic pathways and intracellular signals modulated by a membrane-associated adenylate cyclase. Hyaluronic acid induces sperm capacitation involving LDH and CK activities, thereby reducing oxidative metabolism, and this process is mediated by membrane-associated adenylate cyclase
physiological function
A7BT71
the enzyme contains a BLUF (blue light sensor using flavin) photoreceptor domain that senses blue light using a flavin chromophore, linked to an adenylate cyclase domain. A direct pathway links the conformation of the active site Tyr and Gln to a prominent conserved kink in beta4BLUF and from there to the C-terminal BLUF capping helix. The beta4AC-beta5AC tongue is a central toggle that interacts with a regulatory domain to adjust adenylate cyclase opening and to prepare the active site for catalysis
physiological function
-
PAC shows adenylyl cyclase activity of ATP to cAMP conversion highly stimulated by blue-light exposure and low adenylyl cyclase activity in the dark. Photoexcitation of PAC in its light-adapted signaling state (BLUFs, secondary BLUF domain photocycling) causes high-efficient fast photo-induced Tyr to flavin electron transfer and charge recombination with weak permanent flavin cofactor degradation likely to covalent binding of reduced flavin to protein
physiological function
-
the adenylate cyclase toxin, CyaA, is one of the key virulent factors produced by Bordetella pertussis, the causative agent of whooping cough. This toxin primarily targets innate immunity to facilitate bacterial colonization of the respiratory tract. The adenylate cyclase (AC) catalytic domain of CyaA corresponds to the first 370 residues of the toxin. It binds with high affinity to calmodulin, CaM, a ubiquitous Ca2+-dependent regulator in eukaryotic cells. CaM binding triggers major structural re-arrangements in AC and stimulates its enzymatic activity more than a 1000fold to reach the highest catalytic turnovers known for AC enzymes with a kcat higher than 3000/s in optimal conditions. In the absence of CaM, AC still exhibits a residual activity of 1-3/s, which is on a par with many other AC enzymes
physiological function
adenylyl cyclase (AC) catalyzes the formation of cyclic adenosine monophosphate (cAMP), a canonical second messenger in G protein-coupled receptor (GPCR) signaling that regulates a high number of cellular processes. The nine different membrane-anchored adenylyl cyclase isoforms (AC1-9) in mammals are stimulated by the heterotrimeric G protein Galphas, but their response to Gbetagamma regulation is isoform-specific. For example, AC5 is conditionally activated by Gbetagamma. Human AC5 activity is regulated by various key signaling proteins in addition to Galphas, namely Galphai/o and Gbetagamma3
physiological function
Q7A2D9
light in the near-infrared optical window (NIRW) penetrates deep through mammalian tissues, including the skull and brain tissue. An engineered adenylate cyclase (AC) IlaM5 is activated by NIRW light (NIRW-AC). An approach is undertaken for engineering bacteriophytochromes (Bphs) with non-native, heterologous activities, and design of adenylate cyclases (ACs) activated by NIRW light, NIRW-ACs. Like histidine kinases and diguanylate cyclases, bacterial type III ACs function as homodimers, where conversion of ATP to cAMP takes place at the interface of two monomeric AC domains
physiological function
-
adenylate cyclase toxin (ACT) is a virulence factor secreted by Bordetella pertussis and plays a causative role in whooping cough. After ACT attaches to lung phagocytes, the adenylate cyclase (AC) domain of the toxin is transported into the cytoplasm where it is activated by calmodulin (CaM) to cyclize ATP into 3',5'-cyclic adenosine monophosphate (cAMP). Production of high concentrations of cAMP disrupts immune functions of phagocytes
physiological function
the evolutionarily conserved leucine rich repeat (LRR) protein domain is a unique structural motif found in many viral, bacterial, archaeal, and eukaryotic proteins. The LRR domain serves many roles, including being a signaling domain and a pathogen recognition receptor. In the human innate immune system, it serves an essential role by recognizing fragments of bacterial cell walls. Identification of a stable, membrane-associated peptidoglycan responsive adenylate cyclase LRR domain from human commensal Candida albicans. The human fungal pathogen Candida albicans also uses an LRR domain-containing protein, Cyrp1, to sense bacterial cell wall fragments
physiological function
-
unique domain fusions are seen in adenylyl cyclases from mycobacteria. Characterization of a split gene pair reveals that the adenylyl cyclase has very low activity, representing a pseudoenzyme. The second member of the gene pair harbors an NB-ARC domain that binds adenine nucleotides and a distinct HTH domain that binds DNA and RNA in a sequence-independent manner. In the presence of adenine nucleotides, protein binding to DNA results in the formation of biocrystallized nucleoids. This family of enzymes is found only in slow-growing mycobacteria. Mycobacteria harbor the unique class of adenylyl cyclases with a complex domain organization consisting of an N-terminal putative adenylyl cyclase domain fused to a nucleotide-binding adaptor shared by apoptotic protease-activating factor-1, plant resistance proteins, and CED-4 (NB-ARC) domain, a tetratricopeptide repeat (TPR) domain, and a C-terminal helix-turn-helix (HTH) domain. The products of the rv0891c-rv0890c genes represent a split gene pair, where Rv0891c has sequence similarity to adenylyl cyclases, and Rv0890c harbors the NB-ARC-TPR-HTH domains. Rv0891c has very low adenylyl cyclase activity so it could represent a pseudoenzyme. Atomic force microscopy reveals that binding of Rv0890c to DNA is sequence independent, and binding of adenine nucleotides to the protein induced the formation of higher order structures that may represent biocrystalline nucleoids
physiological function
Adenylyl cyclase (AC) synthesizes the second messenger cAMP, initializing a variety of cell signaling cascades. AC9 contributes to basal cAMP production. Membrane-bound adenylyl cyclase (AC) isoforms have distinct regulatory mechanisms that contribute to their signaling specificity and physiologic roles. Modes of adenylyl cyclase 9 (AC9) regulation include stimulation by Galphas, protein kinase C (PKC) betaII, or calcium-calmodulin kinase II (CaMKII) and inhibition by Galphai/o, PKC isoforms, or calcium-calcineurin. AC9 is directly regulated by Galphas with weak conditional activation by forskolin, other modes of proposed regulation either occur indirectly or possibly require additional scaffolding proteins to facilitate regulation. AC9 regulation by Galphas and Gbetagamma subunits. AC9 is insensitive to direct regulation by Galphai/o in vitro, and AC9 is insensitive to CaMKII and PKCbetaII in vitro
physiological function
adenylate cyclase (AC) is the key enzyme that catalyzes the formation of cAMP from ATP
physiological function
adenylate cyclase (AC) is the key enzyme that catalyzes the formation of cAMP from ATP
physiological function
-
several sensory photoreceptors function as photoactivated adenylyl cyclases (PAC) and hence serve as light-regulated actuators for the control of intracellular levels of 3', 5'-cyclic adenosine monophosphate
physiological function
the adenylyl cyclase (AC) pathway is crucial for pulmonary vasodilation and is inhibited by hypoxia. Forskolin (FSK) binds allosterically to adenylate cyclase, stimulating ATP catalysis. As isozyme AC6 is the primary AC isoform in the pulmonary artery, selective reactivation of AC6 could provide targeted reinstatement of hypoxic AC activity
physiological function
-
adenylyl cyclase is the key catalytic enzyme for the synthesis of 3',5'-cyclic adenosine monophosphate (cAMP). cAMP is an important signaling molecule and the second messenger in animals and lower eukaryotes. It has been confirmed to exist in plant tissues and contributes to multiple biological processes, such as participating in pollen tube growth and reorientation, influencing flowering, responding to biotic and abiotic stresses, promoting tobacco BY-2 cell division, and regulating ion transport with cyclic nucleotide-gated channels. Enzyme MdTTM1 also shows very low phosphohydrolase activity for both organic and inorganic triphosphate substrates
physiological function
-
adenylyl cyclase is the key catalytic enzyme for the synthesis of 3',5'-cyclic adenosine monophosphate (cAMP). cAMP is an important signaling molecule and the second messenger in animals and lower eukaryotes. It has been confirmed to exist in plant tissues and contributes to multiple biological processes, such as participating in pollen tube growth and reorientation, influencing flowering, responding to biotic and abiotic stresses, promoting tobacco BY-2 cell division, and regulating ion transport with cyclic nucleotide-gated channels. Enzyme MdTTM2 also shows phosphohydrolase activity, MdTTM2 shows a powerful hydrolysis capacity for both organic and inorganic triphosphate substrates involving ATP, UTP, CTP, GTP, and triphosphate. Mg2+ rather than Mn2+, which is most helpful for AC activity, assists MdTTM2 to approach its highest ATP hydrolysis activity of 0.48 nmol/min/mg, which is around 5.8 × 104 times higher than its cyclase activity. Mn2+, as the cofactor, can also provide effective support for hydrolyzing ATP. Its catalytic activity reached 0.35 nmol/min/mg
physiological function
-
soluble adenylyl cyclase (sAC) is a HCO3- stimulated enzyme that produces the ubiquitous signalling molecule cAMP, and deems an evolutionarily conserved acid-base sensor. The soluble isozyme sAC is poised to mediate multiple acid-base homeostatic responses in bony fishes. In the presence of carbonic anhydrase, CO2, protons and HCO3- are in a near instantaneous equilibrium, and this enables sAC to act as a general acid-base sensor for multiple physiological processes
physiological function
HpAC1 has substantial triphosphatase activity, indicating the protective activity or a related activity as the protein's physiological function, but the enzyme lacks significant adenylate cyclase activity
physiological function
transmembrane adenylyl cyclases produce the ubiquitous signalling molecule adenosine-39:59-monophosphate (cAMP). Nine genes encode these enzymes in mammals, and each paralogue has unique regulatory properties. Adenylyl cyclase 9 (AC9) is widely distributed in the body and has been implicated in a number of physiological processes, including cardiac function, body fat and body weight, and cancer pathologies and atherosclerosis. The enzyme is autoinhibited by its C-terminal C2b domain, role of the C2b domain and its potential interactions with the coiled-coil, overview
physiological function
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unique domain fusions are seen in adenylyl cyclases from mycobacteria. Characterization of a split gene pair reveals that the adenylyl cyclase has very low activity, representing a pseudoenzyme. The second member of the gene pair harbors an NB-ARC domain that binds adenine nucleotides and a distinct HTH domain that binds DNA and RNA in a sequence-independent manner. In the presence of adenine nucleotides, protein binding to DNA results in the formation of biocrystallized nucleoids. This family of enzymes is found only in slow-growing mycobacteria. Mycobacteria harbor the unique class of adenylyl cyclases with a complex domain organization consisting of an N-terminal putative adenylyl cyclase domain fused to a nucleotide-binding adaptor shared by apoptotic protease-activating factor-1, plant resistance proteins, and CED-4 (NB-ARC) domain, a tetratricopeptide repeat (TPR) domain, and a C-terminal helix-turn-helix (HTH) domain. The products of the rv0891c-rv0890c genes represent a split gene pair, where Rv0891c has sequence similarity to adenylyl cyclases, and Rv0890c harbors the NB-ARC-TPR-HTH domains. Rv0891c has very low adenylyl cyclase activity so it could represent a pseudoenzyme. Atomic force microscopy reveals that binding of Rv0890c to DNA is sequence independent, and binding of adenine nucleotides to the protein induced the formation of higher order structures that may represent biocrystalline nucleoids
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physiological function
-
the Chp chemotaxis-like system regulates intracellular cAMP levels by modulating CyaB activity
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physiological function
-
the enzyme is a key regulator of Pseudomonas aeruginosa virulence
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physiological function
-
unique domain fusions are seen in adenylyl cyclases from mycobacteria. Characterization of a split gene pair reveals that the adenylyl cyclase has very low activity, representing a pseudoenzyme. The second member of the gene pair harbors an NB-ARC domain that binds adenine nucleotides and a distinct HTH domain that binds DNA and RNA in a sequence-independent manner. In the presence of adenine nucleotides, protein binding to DNA results in the formation of biocrystallized nucleoids. This family of enzymes is found only in slow-growing mycobacteria. Mycobacteria harbor the unique class of adenylyl cyclases with a complex domain organization consisting of an N-terminal putative adenylyl cyclase domain fused to a nucleotide-binding adaptor shared by apoptotic protease-activating factor-1, plant resistance proteins, and CED-4 (NB-ARC) domain, a tetratricopeptide repeat (TPR) domain, and a C-terminal helix-turn-helix (HTH) domain. The products of the rv0891c-rv0890c genes represent a split gene pair, where Rv0891c has sequence similarity to adenylyl cyclases, and Rv0890c harbors the NB-ARC-TPR-HTH domains. Rv0891c has very low adenylyl cyclase activity so it could represent a pseudoenzyme. Atomic force microscopy reveals that binding of Rv0890c to DNA is sequence independent, and binding of adenine nucleotides to the protein induced the formation of higher order structures that may represent biocrystalline nucleoids
-
physiological function
-
PAC shows adenylyl cyclase activity of ATP to cAMP conversion highly stimulated by blue-light exposure and low adenylyl cyclase activity in the dark. Photoexcitation of PAC in its light-adapted signaling state (BLUFs, secondary BLUF domain photocycling) causes high-efficient fast photo-induced Tyr to flavin electron transfer and charge recombination with weak permanent flavin cofactor degradation likely to covalent binding of reduced flavin to protein
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physiological function
Thermobifida halotolerans DSM 44931
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adenylate cyclase (AC) is the key enzyme that catalyzes the formation of cAMP from ATP
-
physiological function
Haloactinopolyspora alba DSM 45211
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adenylate cyclase (AC) is the key enzyme that catalyzes the formation of cAMP from ATP
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additional information
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CyaA is a 1706-residue long bifunctional protein made of a CaM-activated catalytic domain (AC) located in the about 400 amino-proximal residues and appended to a 1300-residue long carboxy-terminal moiety that displays all the characteristics of RTX cytolysins. This C-terminal region is indeed endowed with hemolytic activity. The RTX cytolysins are pore-forming toxins that contain characteristic tandem repetitions of nonapeptidic, repeat-in-toxin (RTX) motifs that constitute specific calcium-binding sites. CyaA contains approx. 40 copies of RTX motifs (residues 913-1613)
additional information
Gbetagamma interaction with both purified proteins and cells. The observed interaction is important for motor function. A molecular mechanism wherein Gbetagamma either prevents dimerization of AC5 or allosterically modulates the coiled-coil domain, and hence the catalytic core, is proposed. Detailed structure-function analysis of isozyme AC5
additional information
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although Rv0891c has conserved residues for metal-binding (D97 and D142) and transition-state stabilization (N193 and R197) seen in nucleotidyl cyclases, the protein lacks canonical residues for ATP recognition, substituting an R138 and L186 in place of K and D seen usually in adenylyl cyclases
additional information
ability of isozyme AC9 to heterodimerize with isozymes AC5 and AC6
additional information
three-dimensional enzyme homology structure modeling, using the AC9 cryoEM structure (PDB ID 6R3Q) as a template, and docking, structure-function analysis, overview. The C1 and C2 domains are interconnected and constitute the interface of active and allosteric binding sites. The catalytic moiety and a P-loop accommodate the substrate ATP at the active binding site. In contrast, the allosteric site forms a pocket for forskolin, which activates the AC enzyme
additional information
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computational structure-function prediction and analysis and docking simulation of ATP, catalytic mechanism, overview. The enzyme exhibits typical TTM features and beta-sheets that form a catalytic tunnel. The topologically closed tunnels in MdTTM1 and MdTTM2 are both enclosed by nine anti-parallel beta-sheets, except for two successive beta-sheets, beta4 and beta5, which share the same orientation like having been cut off from one long strand. The alpha-helixes from MdTTM1 and MdTTM2 enzymes show a high consistency. But the beta1 in MdTTM1 is composed of more residues, and MdTTM1 harbors one extra beta-sheet between alpha6 and alpha7 as compared to MdTTM2
additional information
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identification of rtsAC splice variants: isozyme rtsACFL is the longest splice variant, with an ORF of 4953 bp coding a 1650 amino acid protein with a predicted molecular weight of 186 kDa. The N-terminus contains the two catalytic domains C1 and C2 that are essential for cAMP production and bicarbonate stimulation, followed by a STAND nucleotide-binding P-loop motif that also contains three Golgi apparatus targeting sequences. In the most C-terminal region, rtsACFL contains five TPR motifs predicted to mediate protein-protein interactions and the assembly of multiprotein complexes. Variant rtsACT has a 1431 bp ORF that codes for a 476 amino acid and approximately 53 kDa protein, which contains C1 and C2 but none of the C-terminus motifs present in rtsACFL. This rtsAC isoform resembles the mammalian truncated sAC (sACT), rtsACT originates from the retention of the intron after exon 11 that introduces a premature stop codon. rtsACC1a?c code for proteins containing the entire C1 but with partial or absent C2. rtsACC1a codes for a 28 kDa protein that contains exons 1-6, but contains an intron retention before exon 7 that changes the reading frame and introduces a stop codon early in exon 7. This sequence lacks part of the C1 C2 linker and the entire C2. rtsACC1b codes for a 35 kDa protein and originates by alternative 5' SSS at exon 6, skipping of exons 7, 8 and 9 (which code for the C1 C2 linker and part of C2), 3' SSS of exon 10, and intron retention after exon 11 introducing a stop codon. The third C1-only rtsAC variant is rtsACC1c, which codes for a 47 kDa protein that is the result of intron retention after exon 10 that introduces a stop codon. Compared to rtsACT, it lacks exon 11, which is the most C-terminal exon of C2 and contains the residues that bind ATP. rtsACC2 has a 1143 bp ORF and codes for a 43 kDa protein. It skips exons 2 4, which contain residues in C1 essential for binding of catalytic cations, as well as ATP, and HCO3- . It contains exons 5-11, which code for the entire C2 but retains the intron after exon 11, which introduces an early stop codon. Isozyme rtsACC2 contains C2 but lacks most of C1
additional information
the enzyme has generic CYTH architecture
additional information
-
although Rv0891c has conserved residues for metal-binding (D97 and D142) and transition-state stabilization (N193 and R197) seen in nucleotidyl cyclases, the protein lacks canonical residues for ATP recognition, substituting an R138 and L186 in place of K and D seen usually in adenylyl cyclases
-
additional information
-
although Rv0891c has conserved residues for metal-binding (D97 and D142) and transition-state stabilization (N193 and R197) seen in nucleotidyl cyclases, the protein lacks canonical residues for ATP recognition, substituting an R138 and L186 in place of K and D seen usually in adenylyl cyclases
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Show AA Sequence and Transmembrane Helices (23253 entries)
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PDB
SCOP
CATH
UNIPROT
ORGANISM
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MOLECULAR WEIGHT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
103300
I4EC01, I4EC00
x * 103300, isoform AC2, calculated from amino acid sequence
108000
123000
135000
146600
I4EC01, I4EC00
x * 146600, isoform AC8, calculated from amino acid sequence
150000
171000
187000
190000
192000
200000 - 215000
40000
45000
45000 - 54000
46000
48000
49000
50000
75000
81000
x * 81000, deduced from nucleotide sequence, splice variant 1
92000 - 110000
108000
x * 108000, deduced from nucleotide sequence, splice variant 3
187000
full-length enzyme variant
45000
histidine-tagged auto-inhibitory domain Rv1264N, gel filtration
46000
-
1 * 46000, immunoblot, truncated sAC resulting from alternative splicing
46000
-
1 * 46000, immunoblot, truncated sAC resulting from alternative splicing
50000
-
immunoprecipitation, splice variant of the protein, which is the major functional sAC variant in many tissues
50000
testis splice variant
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SUBUNIT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
dimer
heterodimer
homodimer
monomer
additional information
?
x * 108000, deduced from nucleotide sequence, splice variant 3
dimer
adenylate cyclases 2 and 5 can form a functional heterodimeric complex in HEK-293 cells
dimer
histidine-tagged auto-inhibitory domain Rv1264N, gel filtration
dimer
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
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dimer
-
histidine-tagged auto-inhibitory domain Rv1264N, gel filtration
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homodimer
homodimerization of isozyme AC5 might be linked to regulation by Gbetagamma. Dimers of AC5 form in the absence of bound Gbetagamma
monomer
-
1 * 46000, immunoblot, truncated sAC resulting from alternative splicing
monomer
-
1 * 46000, immunoblot, truncated sAC resulting from alternative splicing
additional information
CyaA has two functional domains: the C-terminal domain of about 1300 amino acids, which has membrane-targeting and pore-forming activity, and the 400 amino acid N-terminal domain which has adenylate cyclase enzymatic activity. Intoxication can be triggered by CyaA monomers at low toxin concentrations, whereas cytolytic activity is a co-operative event, mediated by an oligomeric structure consisting of two or more toxin monomers responsible for the production of the pores or channels at higher toxin concentrations
additional information
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CyaA has two functional domains: the C-terminal domain of about 1300 amino acids, which has membrane-targeting and pore-forming activity, and the 400 amino acid N-terminal domain which has adenylate cyclase enzymatic activity. Intoxication can be triggered by CyaA monomers at low toxin concentrations, whereas cytolytic activity is a co-operative event, mediated by an oligomeric structure consisting of two or more toxin monomers responsible for the production of the pores or channels at higher toxin concentrations
additional information
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the AC domain has a modular structure consisting of two subdomains, T25 and T18. The active site is located at the T25/T18 interface. The isolated fragments are completely inactive
additional information
-
tmAC possessses two homologous large cytoplasmic C-terminal domains, C1 and C2, of about 25 kDA each, which are turned to each other in a head-to-tail manner and forming the acive site and the forskolin binding site, the Gs GTP-binding protein and the Gi GTP-binding protein binding sites, the enzyme also possesses a glycosylated transmembrane domain M2
additional information
the enzyme domain structure consists of the Galpha domain, the Ras association domain, the LRR domain, the protein phosphatase 2C domain, and the adenylyl/guanylyl cyclase domain, overview
additional information
detailed structure-function analysis of isozyme AC5
additional information
-
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
-
tmAC possesses two homologous large cytoplasmic C-terminal domains, C1 and C2, of about 25 kDA each, which are turned to each other in a head-to-tail manner and forming the acive site and the forskolin binding site, the Gs GTP-binding protein and the Gi GTP-binding protein binding sites, the enzyme also possesses a glycosylated transmembrane domain M2
additional information
-
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
topology and structure of adenylyl cyclases, mammalian transmembrane adenylyl cyclases share a similar topology of a variable N-terminus and two repeats of a membrane-spanning domain followed by a cytoplasmic domain, the cytoplasmic domains form the catalytic moiety at their interface, creating a pseudosymmetrical site that is primed for bidirectional regulation, crystal structure analysis, overview
additional information
-
tmAC possessses two homologous large cytoplasmic C-terminal domains, C1 and C2, of about 25 kDA each, which are turned to each other in a head-to-tail manner and forming the acive site and the forskolin binding site, the Gs GTP-binding protein and the Gi GTP-binding protein binding sites, the enzyme also possesses a glycosylated transmembrane domain M2
additional information
the soluble isozyme contains two catalytic domains, a C-terminal autoinhibitory domain and leucine zipper, and a P-loop for binding of ATP and GTP
additional information
-
tmAC possessses two homologous large cytoplasmic C-terminal domains, C1 and C2, of about 25 kDA each, which are turned to each other in a head-to-tail manner and forming the acive site and the forskolin binding site, the Gs GTP-binding protein and the Gi GTP-binding protein binding sites, the enzyme also possesses a glycosylated transmembrane domain M2
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POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
acylation
-
CyaA is synthesized as an inactive precursor proCyaA that is converted into an active toxin upon selective acylation of two lysine residues, K860 and K983, a modification that is carried out by a dedicated acyltransferase, CyaC. The acylated CyaA polypeptide is then secreted across the bacterial envelope by a specifc type I secretion machinery (T1SS) made of three components encoded by the cyaB, cyaD, and cyaE genes, which form an operon with the cyaA gene
glycoprotein
phosphoprotein
proteolytic modification
the soluble isozyme is processed by proteases to its active form of 48 kDa
additional information
phosphoprotein
activytion by protein kinase C phosphorylation
phosphoprotein
activation by protein kinase C phosphorylation
phosphoprotein
-
protein kinase A stimulates cAMP in the brain, the activation is increased in brains of patients with bipolar mood disorders, overview
additional information
CyaA is synthesized as a protoxin proCyaA that is post-translationally acylated by a separate protein, CyaC, non-acylated wild-typeroCyaA has no detectable cytotoxic or apoptotic activity
additional information
-
CyaA is synthesized as a protoxin proCyaA that is post-translationally acylated by a separate protein, CyaC, non-acylated wild-typeroCyaA has no detectable cytotoxic or apoptotic activity
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CRYSTALLIZATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
crystal structures of catalytic domains VC1-IIC2 bound to 2'(3')-O-(N-methylanthraniloyl)-GTP, 2'(3')-O-(N-methylanthraniloyl)-ATP, and 2',3'-(2,4,6-trinitrophenyl)-ATP, at 2.9 to 3.3 A resolution, inhibitors reside in the same binding pocket in the VC1-IIC2 protein complex, but there are substantial differences in interactions of base, fluorophore, and polyphosphate chain of the inhibitors with mAC
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crystal structure of the ligand-bound adenylyl cyclase (resulting from the point mutations E497K/C566D) domain at 2.25 A reveals the mechanistic basis for the change from cGMP to cAMP production
purified HpAC1 in complex with a non-hydrolyzable GTP analogue, X-ray diffraction structure determination and analysis, molecular replacement using the protein Q9SIY3 from Arabidopsis thaliana (PDB ID 3V85) as a search model, manual model building
hanging drop vapor diffusion method, using 100 mM sodium acetate (pH 4.8), 200 mM trisodium-citrate, 18% (w/v) PEG 4000, 20% (v/v) glycerol
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in complex with inhibitor bithionol. The inhibitor binds to the isoform Adcy10-specific, allosteric binding site for the physiological activator bicarbonate. Inhibition follows an allosteric mechanism, the compound induces rearrangements of substrate binding residues and of Arg176, a trigger between the active site and allosteric site
complex with 2-hydroxyestradiol and alpha/beta-methylene-ATP, 20-3 A resolution
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2.8 A and 2.9 A resolutions, crystal structures of the complex between stimulatory G protein alpha subunits guanosine 5'-(gamma-thio)triphosphate and the catalytic C1 and C2 domains from type V and type II adenylate cyclase, bound to forskolin and either 2'(3')-O-(N-methylanthraniloyl)-guanosine 5' triphosphate Mg2+ or 2'(3')-O-(N-methylanthraniloyl)-guanosine 5' triphosphate Mn2+
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homology modeling and comparative electrostatic analysis of the catalytic domains of all nine transmembrane adenylate cyclase isoforms providing support for the positioning of the binding site of the inhibitory protein Gialpha at a pseudo-symmetric position to the stimulatory Gsalpha binding site, a structural interpretation of the Gbetacamma interaction with adenylae cyclases 2, 4, and 7 and a new binding site for RGS2
3.3 A resolution active form of the catalytic domain Rv1264, 2.3 A resolution inhibited form
by the hanging-drop, vapour-diffusion method at 18°C, to 1.6 A resolution, crystal structure of the histidine-tagged auto-inhibitory domain Rv1264N shows the protein in a tight, disk-shaped dimer, formed around a helical bundle, and involving a protein chain crossover
crystal structure of the cyclase domain of Rv1900c in the absence and presence of an ATP analogue, active form contains the metal and the nucleotide only at one of the two active sites, two active sites, though exactly identical in sequence, are structurally distinct
crystal structures of Rv1264 holoenzyme in the active and inhibited states, N-terminal domain is alpha-helical and forms a tight platform-like dimer. In the crystal structure of the Rv1900c CHD the residue is not in contact with the ribose moiety of the ATP-analogue alpha,beta-methylene-ATP
Rv1264 crystallized at neutral and acidic pH, CHD activity regulated by dramatic conformational changes
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Rv1625c mutant K296E/F363R/D365C, significant interfacial clashes which preclude dimerization
crystal structure of the tandem GAF domains of CyaB2 shows an antiparallel dimer, in which GAFA of one monomer binds to GAFB of the other and vice versa
Q7A2D9, Q8YVS0, Q8YMH0
crystallographic analysis of PAC in the fully activated state and comparison of the isomorphous light- and dark-state structures. The active site undergoes minimal changes upon light exposure, while enzyme activity may increase up to 50fold
to 1.8 and 2.9 A resolution. Enzyme uses a flavin chromophore within a blue light using flavin (BLUF) domain. A central coiled coil transmits changes from the light-sensing domains to the active sites with minimal structural rearrangement
using 0.1 M 4-morpholineethanesulfonic acid (pH 6.5) and 12% (w/v) polyethylene glycol 20000
crystal structure of native soluble AC and of soluble AC in complex with the competitiv substrate analogs beta-L-2',3'-dideoxyadenosine 5'-triphiosphate and adenosine 5'-(alpha-thio)-triphosphate at 2.8-3.0 A
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crystal structures of catalytic domains VC1-IIC2 bound to 2'(3')-O-(N-methylanthraniloyl)-GTP, 2'(3')-O-(N-methylanthraniloyl)-ATP, and 2',3'-(2,4,6-trinitrophenyl)-ATP, at 2.9 to 3.3 A resolution, inhibitors reside in the same binding pocket in the VC1-IIC2 protein complex, but there are substantial differences in interactions of base, fluorophore, and polyphosphate chain of the inhibitors with mAC
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fusion between Deinococcus radiodurans bacteriophytochrome linked to Synechocystis sp. guanylate/adenylate cyclase, to 2.35 A resolution. Light-induced conformational changes in the phytochrome destabilize the coiled-coil sensor-effector linker, which releases the cyclase regulatory element from an inhibited conformation, increasing cyclase activity of the artificial system
A0A068MZJ9
hanging drop vapor diffusion, 0.001 ml protein solution containing 4 mg/ml GRESAG4.1 in 5 mM Tris-HCl, pH 8.0 is mixed with either 1.8-1.9 M ammonium sulfate, pH 6.5 and pH 7.75 or 1.2 M sodium citrate at pH 5.4, crystals diffract to 1.9-2.1 A resolution
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at 1.9 A resolution, crystals belong to space group P212121, eight highly conserved ionic residues, E10, E12, K14, R63, K76, K111, D126, and E136 lie in the barrel core and form the likely binding sites for substrate and divalent cations. A phosphate ion bound to R63, K76, K111, and R113 near the center of the conserved cluster. AC-IV active site is relatively enriched in glutamate and features an ExE motif as its most conserved element
Q7CH76
by vapour diffusion-hanging drop method, amino-terminal His-tagged construct, from which the tag was removed by thrombin, crystallized in a triclinic form diffracting to 1.9 A resolution, with one dimer per asymmetric unit and unit-cell parameters a = 33.5, b = 35.5, c = 71.8 A, alpha = 88.7, beta = 82.5, gamma = 65.5°. Non-His tagged native construct crystallized in space group P212121 with unit-cell parameters a = 56.8, b = 118.6, c = 144.5 A, to 2.9 A resolution and probably having two dimers per asymmetric unit
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PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
more |
replacement of the entire beta1-beta3 region, Ile250 to Ile283, of the cyaB1 GAF B subdomain with Asn411 to Tyr443 of GAF B from rat phosphodiesterase 2, is stimulated by cGMP 10.5fold similar to wild-type cyaB1, whereas activation by cAMP is eliminated, thus switched specificity of the cyaB1 tandem GAF domain from cAMP to cGMP. Swapping of the anterior part, Ile250 to Gly267, in cyaB1 GAF B with Asn411 to Asn426 of rat phosphodiesterase 2, which is stimulated by neither cAMP nor cGMP up to 10 mM. Swapping the C-terminal W270 to I283 section of cyaB1 for Val429 to Tyr443 from rat phosphodiesterase 2 yields a protein that is highly stimulated by both cAMP and cGMP, i.e. purine specificity is lost. Elongation of the swapped stretch of amino acids towards the N-terminal, e.g. when Thr258/Leu259 are included in the domain swapping and replaced by Ser and Val cNMP, specificity is inverted, i.e. the efficacy of cAMP is almost lost, whereas cGMP stimulates cyaB1 AC potently
T258S
preference for cGMP over cAMP is 35fold, affinity for both cyclic nucleotides is enhanced
K372A
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mutant with 30fold reduced catalytic rate constant and 3fold increased Km value for ATP
N347A
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the mutant shows an enzymatic activity that is reduced by about half as well as 5fold reduced affinity for calmodulin
Q260A/R262A
a CyaA 1-373 mutant, the mutant shows reduced calmodulin-dependent activation of CyaA compared to the wild-type CyaA
Q260C
the mutant shows about 1000fold reduced potency to be activated by calmodulin compared to the wild-type CyaA
R338A/D360A
-
the mutant shows no affected catalytic efficiency but 6fold reduced affinity for calmodulin
R338A/N347A/D360A
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the mutant shows 15% of wild type turnover and exhibits 200fold reduced affinity for calmodulin
V1027A/L1031A
is not catalytically active under basal, Galphas- or forskolin-stimulated conditions
E497K/C566D
D114A
site-directed mutagenesis, the almost inactive mutant shows highly reduced activity compared to the wild-type enzyme
D116A
site-directed mutagenesis, the almost inactive mutant shows highly reduced activity compared to the wild-type enzyme
D300A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
E185A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
E242A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
K136A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
K253A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
K260A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
K264A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
K332A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
R19A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
S103A
site-directed mutagenesis, the mutant has a 17fold higher Km for ATP compared to the wild-type enzyme, and the mutation causes a marked reduction of discrimination between ATP- and ADP- or AMP-derived inhibitors
S106A
site-directed mutagenesis, the mutation reduces the mutant activity to 25% of the wild-type enzyme activity, kinetic analysis show a 58% reduction of the Vmax and a doubling of the Km compared to the wild-type enzyme
S113A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
T189A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
W118A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
W200A
site-directed mutagenesis, the mutant shows highly reduced activity compared to the wild-type enzyme
W249A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
W374A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
Y394A
site-directed mutagenesis, the mutant shows reduced Vmax and altered Km compared to the wild-type enzyme
E166A
site-directed mutagenesis, adenylate cyclase catalytically inactive mutant with reduced PPPase activity compared to wild-type
E2A
site-directed mutagenesis, adenylate cyclase catalytically inactive mutant with reduced PPPase activity compared to wild-type
R52A
site-directed mutagenesis, adenylate cyclase catalytically inactive mutant with reduced PPPase activity compared to wild-type
A726T
naturally occuring mutation, the single nucleotide polymorphism is associated with familial dyskinesia and is a gain-of-function mutation
D1015E
naturally occuring mutation, the single nucleotide polymorphisms (SNPs) Y233H within N-alpha3, which packs against the coiled-coil domain, and D1015E within the coiled-coil domain are correlated to neurological disorders and can affect the packing of the coiled-coil domain and consequently modulation of the catalytic core
E326D
site-directed mutagenesis, the mutation E326D causes a 10fold increase in basal cAMP production and an enhancement of the cAMP response to isoproterenol. The mutation reduces the efficacy of the enzyme's C2b domain to quench the activation of AC9 by Gs-coupled receptors (GsRs)
M1029K
naturally occuring mutation, the single nucleotide polymorphism is associated with familial dyskinesia and is a gain-of-function mutation. The mutant has similar maximal responsiveness but a right shift in the EC50 value compare to wild-type
N503A
site-directed mutagenesis, the mutation decreases the forskolin-stimulated adenylate cyclase activity, while the hypoxia sensitivity of the mutant is unaltered compared to wild-type enzyme
R418W
naturally occuring mutation, the single nucleotide polymorphism is associated with familial dyskinesia and is a gain-of-function mutation. The mutant has significantly reduced AC5 activation by Gbetagamma and dramatically higher EC50 value
S1035A
site-directed mutagenesis, the mutation decreases the forskolin-stimulated adenylate cyclase activity, while the hypoxia sensitivity of the mutant is unaltered compared to wild-type enzyme
T500A
site-directed mutagenesis, the mutation decreases the forskolin-stimulated adenylate cyclase activity, while the hypoxia sensitivity of the mutant is unaltered compared to wild-type enzyme
Y233H
naturally occuring mutation, the single nucleotide polymorphisms (SNPs) Y233H within N-alpha3, which packs against the coiled-coil domain, and D1015E within the coiled-coil domain are correlated to neurological disorders and can affect the packing of the coiled-coil domain and consequently modulation of the catalytic core
K533E/I603R/D605C
mutant lose adenylyl cyclase activity but obtains significant guanylyl cyclase activity
D147A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1647 mutant, mutation of first metal-binding residue, barely active
D241C
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
D256A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of the metal-binding residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
D256A/D300A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
mixture of artificial C2-like mutants of Rv1625c, reconstitutes an active enzyme
D300A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of the metal-binding residue, leads to significant decrease in adenylyl cyclase activity, can heterodimerize and reconstitute activity with the Paramaecium guanylyl cyclase C1-like domain, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
D365A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of the substrate specifying residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
D365C
E136A
shift of the pH optimum by about 0.5 unit to acidic pH
E136R
shift of the pH optimum by about 0.5 unit to acidic pH
E195A
mutation with partially relieved inhibition and 4fold increased enzyme activity at pH 8.0, pH optimum shifted from 5.8 to 6.5
F363R
H103A
pH regulation is barely affected, not involved in pH-regulation
H140A
pH regulation is barely affected, not involved in pH-regulation, shift of the pH optimum by about 0.5 unit to acidic pH
H140R
inhibition is relaxed slightly, with a shift of the pH optimum toward more basic values
H192A
mutant with wild-type phenotype at pH 8.0, the slope of activation is shifted by 0.5 pH units towards the acidic pH. 10fold higher enzyme activity at pH 8.0 than the wild type
H58A
pH regulation is barely affected, not involved in pH-regulation
K187E
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
K187E/D241C
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1647 mutant, mixture of artificial C1-like mutants, reconstitutes high adenylyl cyclase activity, does not lead to a gain in guanylyl cyclase activity
K296A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of the substrate specifying residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
K296A/D365A/R376A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
mixture of artificial C1-like mutants of Rv1625c, reconstitutes an active enzyme
K296E
K296E/D365C
K296E/F363R/D365C
Q57K/N106D
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv0386 mutant, abolishes activity
R132A
shift of the pH optimum by about 0.5 unit to acidic pH
R132E
results in a biphasic pH activity curve with a minimum at pH 6.5 and higher activity at basic pH values
R18A
88% of wild-type activity, in the presence of 2 mM Mn2+
R18A/R19G
67% of wild-type activity, in the presence of 2 mM Mn2+
R19G
78% of wild-type activity, in the presence of 2 mM Mn2+
R27A
78% of wild-type activity, in the presence of 2 mM Mn2+
R31G
118% of wild-type activity, in the presence of 2 mM Mn2+
R376A
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of the transition state stabilizing residue, leads to significant decrease in adenylyl cyclase activity
R43A
61% of wild-type activity, in the presence of 2 mM Mn2+
R43A/R44G
R43K
77% of wild-type activity, in the presence of 2 mM Mn2+
R43K/R44K
39% of wild-type activity, in the presence of 2 mM Mn2+
R44G
41% of wild-type activity, in the presence of 2 mM Mn2+
R44K
116% of wild-type activity, in the presence of 2 mM Mn2+
R46A
85% of wild-type activity, in the presence of 2 mM Mn2+
R46K
135% of wild-type activity, in the presence of 2 mM Mn2+
R4G
77% of wild-type activity, in the presence of 2 mM Mn2+
D147A
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Rv1647 mutant, mutation of first metal-binding residue, barely active
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D241C
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Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
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D256A
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Rv1625c mutant, mutation of the metal-binding residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
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D300A
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Rv1625c mutant, mutation of the metal-binding residue, leads to significant decrease in adenylyl cyclase activity, can heterodimerize and reconstitute activity with the Paramaecium guanylyl cyclase C1-like domain, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
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D365A
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Rv1625c mutant, mutation of the substrate specifying residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
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E195A
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mutation with partially relieved inhibition and 4fold increased enzyme activity at pH 8.0, pH optimum shifted from 5.8 to 6.5
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H103A
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pH regulation is barely affected, not involved in pH-regulation
-
H140A
-
pH regulation is barely affected, not involved in pH-regulation, shift of the pH optimum by about 0.5 unit to acidic pH
-
H140R
-
inhibition is relaxed slightly, with a shift of the pH optimum toward more basic values
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H192A
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mutant with wild-type phenotype at pH 8.0, the slope of activation is shifted by 0.5 pH units towards the acidic pH. 10fold higher enzyme activity at pH 8.0 than the wild type
-
H58A
-
pH regulation is barely affected, not involved in pH-regulation
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K187E
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Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
-
K187E/D241C
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Rv1647 mutant, mixture of artificial C1-like mutants, reconstitutes high adenylyl cyclase activity, does not lead to a gain in guanylyl cyclase activity
-
K296A
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Rv1625c mutant, mutation of the substrate specifying residue, leads to significant decrease in adenylyl cyclase activity, can not reconstitute activity with C1 or C2 domains of the mammalian adenylyl cyclase isoforms or with Rv1647
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K296E/D365C
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double mutant with severely compromised enzyme activity
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K296E/F363R/D365C
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triple mutant with severely compromised enzyme activity
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R18A/R19G
-
67% of wild-type activity, in the presence of 2 mM Mn2+
-
R376A
-
Rv1625c mutant, mutation of the transition state stabilizing residue, leads to significant decrease in adenylyl cyclase activity
-
R43A/R44G
-
1.3% of wild-type activity, in the presence of 2 mM Mn2+
-
A197T
the mutant shows increased activity compared to the wild type enzyme
E189R
the mutant shows increased activity compared to the wild type enzyme
E377G
the mutant shows increased activity compared to the wild type enzyme
F399H
the mutant shows increased activity compared to the wild type enzyme
F399I
the mutant shows increased activity compared to the wild type enzyme
I352T
the mutant shows increased activity compared to the wild type enzyme
L326P
the mutant shows increased activity compared to the wild type enzyme
r23ExoY
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mutant with histidine tag at carboxyl-terminal position, detectable enzyme activity
R318W
the mutant shows increased activity compared to the wild type enzyme
R412H
the mutant shows slightly increased activity compared to the wild type enzyme
R456L
the mutant shows strongly increased activity compared to the wild type enzyme
rExoY
-
mutant with histidine tag at amino-terminal position, detectable enzyme activity
E189R
-
the mutant shows increased activity compared to the wild type enzyme
-
E377G
-
the mutant shows increased activity compared to the wild type enzyme
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F399I
-
the mutant shows increased activity compared to the wild type enzyme
-
L326P
-
the mutant shows increased activity compared to the wild type enzyme
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R318W
-
the mutant shows increased activity compared to the wild type enzyme
-
D425A
-
catalytically inactive mutant of isoform AC6, the expression of the mutant is associated with marked reduction in cAMP production
C83A
Q7CH76
the mutation results in moderate to sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
D55K
Q7CH76
the mutant shows increased Km for Mg2+ compared to the wild type enzyme
E10A
E10Q
Q7CH76
the mutation results in about 8fold reduction in activity with 20 mM Mg2+ and in a 5fold increase in activity in the presence of 10 mM Mn2+
E12Q
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
E136A
E84A
-
gives crystals that are unsuitable owing to poor crystal growth or poor diffraction
F5A
Q7CH76
the mutant shows increased Km for Mg2+ compared to the wild type enzyme
K14A
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
K76A
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
L72A
Q7CH76
the mutant shows about 2fold increased Km for Mg2+ compared to the wild type enzyme
M140A
Q7CH76
the mutation results in moderate to sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
R113A
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ and no activity with Mg2+
R63A
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
additional information
E497K/C566D
mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclases
E497K/C566D
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mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclases
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D365C
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0.06% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
D365C
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
F363R
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
K296E
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0.5% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
K296E
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
K296E/D365C
-
0.025% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
K296E/D365C
double mutant with severely compromised enzyme activity
K296E/F363R/D365C
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0.5% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
K296E/F363R/D365C
triple mutant with severely compromised enzyme activity
K296E/F363R/D365C
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, is largely monomeric, has neither adenylyl cyclase or guanylyl cyclase activity, unable to heterodimerize with the wild-type protein
R43A/R44G
1.3% of wild-type activity, in the presence of 2 mM Mn2+
R43A/R44G
P9WQ35, O06362, P71914, P94982, P9WMU7, P9WMV1, O06572, P9WM05, O07732, O53720, Q11028, O53213, P9WQ33, P9WQ31, P9WQ29
Rv1625c mutant, mutation of two arginine residues in the extreme N-terminal region, preceding the first transmembrane helix, severely compromises adenylyl activity of the full length protein
E10A
-
gives crystals that are unsuitable owing to poor crystal growth or poor diffraction
E10A
Q7CH76
the mutation results in about 8fold reduction in activity with 20 mM Mg2+ and in a 5fold increase in activity in the presence of 10 mM Mn2+
E136A
-
gives crystals that are unsuitable owing to poor crystal growth or poor diffraction
E136A
Q7CH76
the mutation results in sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
additional information
A7BT71
a series of engineered, optogenetic, spatially-restricted, photoactivable adenylyl cyclases (PACs) positioned at the plasma membrane (PM), the outer mitochondrial membrane (OMM), and the nucleus (Nu) is constructed, phenotypes, detailed overview. Enzyme engineering: the mitochondrial localization sequence (MLS) is derived from the first 30 amino acids of AKAP1, the PM targeting sequence from the K-Ras CAAX, and the nuclear localization sequence (NLS) from the SV40 large T antigen NLS. In addition, the fluorescent protein mCherry is fused to the N-terminus of bPAC in all constructs to assist in visualizing localization. These constructs are introduced into a lentiviral vector under control of the MCSV 5' LTR promoter for moderate levels of expression. Stable MVD7 cell lines are generated via lentiviral transduction and subsequently enriched by fluorescence activated cell sorting (FACS). Prolonged cAMP generation at the OMM profoundly stimulates nuclear PKA activity. Phosphodiesterases 3 (OMM and PM) and 4 (PM) modulate proximal (local) cAMP-triggered activity, whereas phosphodiesterase 4 regulates distal cAMP activity as well as the migration of PKA's catalytic subunit into the nucleus
additional information
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engineering of photoactivated adenylyl cyclases (PACs), method development and evaluation, detailed overview. Cyclase activity is monitored in bacterial cells via expression of a fluorescent reporter, and programmable illumination allows the rapid exploration of multiple lighting regimes. Probing of two PACs responding to blue and red light, respectively. Significant dark activity is observed for both. Engineered derivatives of the red-light-sensitive PAC with altered responses to light, with one variant, denoted DdPAC, showing enhanced response to light. These PAC variants stand to enrich the optogenetic toolkit and thus facilitate the detailed analysis of cNMP metabolism and signaling. Analysis and optimization of the performance of PACs
additional information
-
downregulation of the cyaA gene leads to reduced virulence of the organism, e.g. strain 253, in C57BL/6 mice, overview. The cya locus, which encodes, activates, and secretes CyaA, is replaced by an operon ptp, predicted to encode peptide transport proteins, in strain 253, genotyping and phylogenetic analysis, overview
additional information
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mutants lacking either filamentous haemagglutinin or ACT (strain Bp3183) show significantly decreased adherence to human epithelial respiratory cells, lack of ACT does not affect filamentous haemagglutinin cellular expression, attachment level of the ACT-deficient mutant to A549 cells is not affected by the presence of heparin
additional information
the CyaA mutant with a Cys/Thr insertion at amino acids 188/189 is unable to kill J774 mouse macrophage-like cells at a concentration as high as 0.010 mg/ml, yet lytic activity towards erythrocytes is retained. Binding of a monoclonal antibody distal to the inactivated catalytic site restored cytotoxicity towards J774 cells and further enhances haemolytic activity, construction of mutant CyaA* lacking adenylate cyclase enzymatic activity, and of non-acylated forms of wild-type CyaA and mutant CyaA*, proCyaA and proCyaA*, CyaA* is as cytotoxic towards J774.2 cells as CyaA and mediates cell killing at a faster rate than CyaA at higher concentration than 0.0001 mg/ml. Non-acylated mutant proCyaA* has no detectable cytotoxic or apoptotic activity. A 500fold higher concentration of non-acylated or mutant CyaA is necessary for inhibition of the zymosan-stimulated oxidative burst
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the CyaA mutant with a Cys/Thr insertion at amino acids 188/189 is unable to kill J774 mouse macrophage-like cells at a concentration as high as 0.010 mg/ml, yet lytic activity towards erythrocytes is retained. Binding of a monoclonal antibody distal to the inactivated catalytic site restored cytotoxicity towards J774 cells and further enhances haemolytic activity, construction of mutant CyaA* lacking adenylate cyclase enzymatic activity, and of non-acylated forms of wild-type CyaA and mutant CyaA*, proCyaA and proCyaA*, CyaA* is as cytotoxic towards J774.2 cells as CyaA and mediates cell killing at a faster rate than CyaA at higher concentration than 0.0001 mg/ml. Non-acylated mutant proCyaA* has no detectable cytotoxic or apoptotic activity. A 500fold higher concentration of non-acylated or mutant CyaA is necessary for inhibition of the zymosan-stimulated oxidative burst
additional information
upon insertion of the N-terminal adenylyl cyclase domain of Bordetella pertussis CyaA to its targeted eukaryotic cells, target cell calmodulin binds to this domain tightly with high affinity, the interaction activates the adenylyl cyclase activity of CyaA leading to a rise in intracellular cAMP levels to disrupt normal cellular signaling, the complex formation between N-CaM and CyaA contributes a 400fold increase of binding affinity between CyaA and CaM
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upon insertion of the N-terminal adenylyl cyclase domain of Bordetella pertussis CyaA to its targeted eukaryotic cells, target cell calmodulin binds to this domain tightly with high affinity, the interaction activates the adenylyl cyclase activity of CyaA leading to a rise in intracellular cAMP levels to disrupt normal cellular signaling, the complex formation between N-CaM and CyaA contributes a 400fold increase of binding affinity between CyaA and CaM
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CyaA causes similar morphological changes in various cultured cell lines: L2, EBL, HEK293T, MC3T3-E1, NIH 3T3, and Vero cells are rounded by the toxin whereas Caco-2, Eph4, and MDCK cells are not, although all these cells show a significant elevation of the intracellular cAMP level in response to CyaA treatment. An inactive enzyme mutant does not cause cell form modifications in infected rats in contrast to the wild-type enzyme, overview
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Bordetella pertussis adenylate cyclase toxin CyaA is engineered as a potent vaccine vehicle to deliver antigens into antigen-presenting cells, while the adenylate cyclase catalytic domain has been used to design a robust genetic assay for monitoring protein-protein interactions in bacteria. Monitoring protein-protein interactions in vivo in Escherichia coli via the bacterial adenylate cyclase-based two-hybrid (BACTH) system. In an Escherichia coli cya strain, the T25 and T18 fragments of CyaA are co-expressed as fusions with polypeptides X and Y; interaction between X and Y triggers heterodimerization of the hybrid proteins leading to cAMP synthesis. The catabolite activator protein (CAP) binds cAMP and activates transcription of catabolic operons (reporter gene)
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mutants lacking either filamentous haemagglutinin or ACT (strain Bp3183) show significantly decreased adherence to human epithelial respiratory cells, lack of ACT does not affect filamentous haemagglutinin cellular expression, attachment level of the ACT-deficient mutant to A549 cells is not affected by the presence of heparin
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additional information
ACI-deletion mutants ACI.lambda1057 with reduced catalytic activity and ACI.lambda1094, which like mutant ACIlambda1057 is active and stimulated by Ca/CaM as well as ACI. Mutant ACII.lambda928 is catalytically inactive, mutant ACII.AA930 shows diminished activity, mutants ACII.AA925 or ACII.AA932 show no significant change in Gbetagamma-regulation
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construction of a mutant strain expressing a version of Cyr1p with an N-terminal His-Flag-Myc tag under the control of the MET3 promoter
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development of optimal recombinant expression workflows for the entire region of the LRR domain of Cyr1p as a peripheral membrane protein. Design of a peptidoglycan enrichment bead assay, the LRR domain can bind bacterial peptidoglycan fragments under native conditions. The membrane-associated Cyr1p-LRR construct sets the stage for the development of antifungal agents via high-throughput campaigns to inhibit cell wall-Cyr1p interactions
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deletion of a 12TM domain of ACA, does not perturb cAMP secretion
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aca-/rdeA- mutant cells with significant activity of ACB, which is not obscured by the presence of ACA, aca-/A15::ACG mutant cells, which express ACG
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the learning mutant rutabaga, i.e. rut, shows reduced synaptic strength and precision compared to the wild-type enzyme, rut motor terminals display greatly increased variability among corresponding terminal branches of different larval neuromuscluar junctions of different samples, defects in rut adenylyl cyclase results in reduced Ca2+ currents in the nerve terminal, phenotype, overview
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RNAi against gene AC78C, but not against gene ACXE, depressed the sucrose response in gustatory receptor neurons
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mutant ACVIdeltaN, shows a much lower activity as compared with full-length ACVI, but its stimulated activity is about 4fold higher than the corresponding control activity, activities of the recombinant, engineered, soluble forms of ACV and ACVI, which lack the N termini, are not enhanced by Gbetagamma subunits. Deletion of residues 77-151, but not 1-76, in the N-terminal region of ACVI obliterates the ability of Gbetagamma subunits to conditionally stimulate the enzyme
additional information
AC7AC3 chimeric mutants, exchange of the putative transmembrane domains, M1 and M2 or of the N-terminal tail has no effect on the ethanol response of enzyme activity
additional information
RNAi is used to knockdown each of the four AC isozymes AC2, AC3, AC7, and AC9 specifically and individually in RAW 264.7 cells, bone marrow-derived macrophage from AC7 knockout mice are devoid of an sphingosine 1-phosphate effect on cAMP stimulated by Gs-dependent pathways, but exogenous expression of AC7, while not of AC2, is sufficient to recapitulate the sphingosine 1-phosphate/G13 effect on intracellular cAMP responses. Regulation of the Gs-stimulated cAMP responses by the Gi and Gq/Ca2+ pathways is affected in AC7-deficient cells, overview
additional information
RNAi is used to knockdown each of the four AC isozymes AC2, AC3, AC7, and AC9 specifically and individually in RAW 264.7 cells, bone marrow-derived macrophage from AC7 knockout mice are devoid of an sphingosine 1-phosphate effect on cAMP stimulated by Gs-dependent pathways, but exogenous expression of AC7, while not of AC2, is sufficient to recapitulate the sphingosine 1-phosphate/G13 effect on intracellular cAMP responses. Regulation of the Gs-stimulated cAMP responses by the Gi and Gq/Ca2+ pathways is affected in AC7-deficient cells, overview
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sixteen single-nucleotide polymorphisms distributed throughout the ADCY10 gene are genotyped in two healthy groups of American whites: 1692 premenopausal women and 715 men, genotype association with bone mineral density phenotypes, overview
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construction of various truncated versions of isozyme AC6 lacking parts of the C-terminal domains C1 or C2, localization of the structural features required for interaction with lipid rafts, overview
additional information
many SNPs involve residues located near the Gbetagamma binding interface. Among them, R418W, A726T, M1029K, and DELTA9bp are associated with familial dyskinesia and represent gain-of-function mutations. Gbetagamma affects the AC activity of R418W, M1029K, and DELTA9bp expressed in HEK-ACDELTA3/6 cell membranes. All exhibit significant defects in Gbetagamma activation. R418W and DELTA9bp have significantly reduced AC5 activation by Gbetagamma and dramatically higher EC50 values
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model-guided site-directed mutagenesis of selected residues at the allosteric activator (FSK) binding site (T500, N503, S1035)
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mutation of either His572 or Asp895 greatly reduces AC activity
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sAC-/- spermatozoa, adenylyl cyclase activity and cAMP content are greatly diminished and are undetectable after sperm purification. HCO3- is unable to rapidly accelerate the flagellar beat or facilitate evoked Ca2+ entry into sAC-/- spermatozoa. However, sAC-/- sperm fertilize zona-free oocytes
additional information
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AC5-deficient (AC5-/-) mice, reduction of basal L-type Ca2+ currents is significantly less pronounced than in wild-type myocytes, isoproterenol effects on L-type Ca2+ currents are mitigated
additional information
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mice with collecting duct-specific deletion of endothelin-1, mRNA or protein levels of AC3 not affected, increased protein levels of AC5/6, AC5 and AC6 mRNA levels are unchanged, show enhanced vasopressin-stimulated cAMP accumulation
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mice deficient in AC1, are resistant to glutamate-induced neuronal toxicity, double knock-out AC1 and AC8 mice, show long lasting long-term potentiation and memory deficits that are greater in animals lacking both AC1 and AC8, when compared to animals deficient in only a single isoform. Behavioral responses to inflammatory stimuli that appear to involve N-methyl-D-aspartate receptor pathways are markedly reduced in double knockouts and AC1-/- mice. AC1-/- mice are resistant to glutamate-induced neuronal toxicity
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deletion of sAC, leads to inhibition of sperm mobility, animals are infertile, AC3 knockout mice, exhibit peripheral and behavioral anosmia
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AC5-/- mice, all of the major behavioral effects of morphine, including locomotor activation, analgesia, tolerance, reward, and physical dependence and withdrawal symptoms, are attenuated. Sniffing, ptosis, teeth chattering, and body tremor are markedly reduced, diarrhea and paw tremor are not significantly different, the number of jumps is dramatically increased. Behavioral effects of selective micro or delta opioid receptor agonists are lost, behavioral effects of selective kappa opioid receptor agonists are unaffected. Loss of AC5 does not alter expression levels of opioid receptor transcripts
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knockout of sAC in mice causes male sterility by impaired sperm motility, while spermatogenesis is not affected
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transgenic mice that express a mutant, constitutively active inhibitory G protein, Galpha12, in principal neurons of the forebrain, show markedly enhanced long-term depression and impaired late-phase long-term potentiation at Schaffer collateral synapses, with no associated differences in input/output relations, paired-pulse facilitation, or NMDA receptor-gated conductances
additional information
generation of transgenic mice with disrupted AC5 or overexpressing AC5, the latter type shows less decreased heart rate in later phases within one parabola, the inverse heart rate is more variable in AC5 knockout mice and less variable in AC5 overexpressing mice compared to wild-type mice, overview
additional information
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generation of transgenic mice with disrupted AC5 or overexpressing AC5, the latter type shows less decreased heart rate in later phases within one parabola, the inverse heart rate is more variable in AC5 knockout mice and less variable in AC5 overexpressing mice compared to wild-type mice, overview
additional information
sperm from Sacy null mice are immotile or weakly motile, but their motility is activated by the cAMP analogues N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate and adenosine 3',5'-cyclic monophosphate acetoxymethyl ester activated motility. Ca2+ cannot substitute for cAMP analogues in activating motility in the mutant, overview
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the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC1 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, phenotypes, overview
additional information
the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC1 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, phenotypes, overview
additional information
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Adcy1-/- mice lack the type 1 adenylyl cyclase, no compensatory changes in the levels of transcripts encoding the related type 8 adenylyl cyclase isoform in retinas of mice deficient in AC1, phenotype of AC1-deficient mice, overview. A dysfunction of Ca2+/CaM-stimulated adenylyl cyclase activity in Drd4-/-mouse retina appears to be due primarily to low levels of expression of the AC1 and not to changes in CaM expression
additional information
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mice lacking AC5 display strong reductions in anxiety-like behavior in several paradigms. This anxiolytic behavior in AC5-deficient mice is reduced by the D1 receptor antagonist SCH23390 and enhanced by the D1 dopamine receptor agonist, dihydrexidine or DHX. DHX-stimulated c-fos induction was enhanced in the dorso-medial striatum and NAc in AC5-deficient mice, phenotype, overview. siRNA-mediated inhibition of AC5 levels within the NAc is sufficient to produce an anxiolytic-like response, causing upregulation of prodynorphin and downregulation of cholecystokinin in the NAc of AC5-deficient mice, the effect is reversible by administration of nor-binaltorphimine, a kappa opioid receptor antagonist, or CCK-8s, a CCK receptor agonist, overview
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in cells from mice doubly deficient in isozymes AC1 and AC8, the baseline percentage of active synapses is only modestly reduced compared with wild-type synapses, and forskolin unsilencing is similar in the two genotypes, but after strong presynaptic silencing, recovery of normal function is strongly inhibited in AC1/AC8-deficient synapses, the entire recovery phenotype of the double null is reproduced in AC8-deficient but not in AC1-deficient cells, overview
additional information
construction of sAC knock-out mice containing an internal ribosome entry site-LacZ/neomycin cassette that replaces exons 2-4, deleting sequence encoding a portion of the C1 domain of sAC, the C1 domain combines with C2 to form the cyclase catalytic domain. RNA transcription proceeds through the inserted IRES-LacZ/neomycin cassette and mRNAencoding C2 is produced, but not the C1 region in testis of adult sAC-null mice, but due to the frameshift of the transgene intro the C2 portions of sAC are not translated and neither sAC protein nor its activity are detectable in testis and spermatozoa of knock-out animals, overview. sAC-null mice do not exhibit any obvious neurological deficits
additional information
increase of Fmr1 mRNA is attenuated in ACC slices from AC1 KO mice compared to wild-type mice, and induced phosphorylation of CREB is significantly attenuated in ACC slices from AC1 KO mice compared with WT mice
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increase of Fmr1 mRNA is attenuated in ACC slices from AC1 KO mice compared to wild-type mice, and induced phosphorylation of CREB is significantly attenuated in ACC slices from AC1 KO mice compared with WT mice
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AC1 mutant mouse, barrelless, lacks typical barrel cytoarchitecture, and displays presynaptic and postsynaptic functional defects at thalamocortical synapses, in which LTP induction and the developmental increase in AMPA receptor response at thalamocortical synapses are impaired. The barrel cortex phenotype of brl mice may be a consequence of AC1 disruption in cortical or subcortical regions
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mice overexpressing AC1 show superior remote contextual memory even though they exhibit normal hippocampus-dependent contextual memory, AC1 knockout mice show lower remote memory 11 weeks, but not within the first 5 weeks, after training compared with wild-type mice, phenotypes, overview
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construction of AC1 and AC1/8 double knockout mice, AC1 knockout mice exhibit reduced opiate, e.g. morphine, dependence on the basis of attenuated withdrawal, however, partially distinct withdrawal symptoms are affected in the two lines. The ability of chronic morphine to enhance the effect of forskolin on LC firing rates is completely abolished in AC8 and AC1/8 deficient mutants, morphine regulation of gene expression in locus coeruleus of AC1 KO mice, overview
additional information
construction of AC1 and AC1/8 double knockout mice, AC1 knockout mice exhibit reduced opiate, e.g. morphine, dependence on the basis of attenuated withdrawal, however, partially distinct withdrawal symptoms are affected in the two lines. The ability of chronic morphine to enhance the effect of forskolin on LC firing rates is completely abolished in AC8 and AC1/8 deficient mutants, morphine regulation of gene expression in locus coeruleus of AC1 KO mice, overview
additional information
construction of male and female AC1/8 double knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
construction of male and female AC1/8 double knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
construction of male and female AC1/8 double knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
construction of a chimeric mutant dimer of AC2/AC5, which shows increased activation by GalphaS proteins as compared to the single isozymes AC2 and AC5, expression of the chimeric dimer elevates cAMP production in transfected cells 6fold, while that of the single isozymes each cause a 2fold increase in cAMP production, overview
additional information
construction of a chimeric mutant dimer of AC2/AC5, which shows increased activation by GalphaS proteins as compared to the single isozymes AC2 and AC5, expression of the chimeric dimer elevates cAMP production in transfected cells 6fold, while that of the single isozymes each cause a 2fold increase in cAMP production, overview
additional information
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construction of a chimeric mutant dimer of AC2/AC5, which shows increased activation by GalphaS proteins as compared to the single isozymes AC2 and AC5, expression of the chimeric dimer elevates cAMP production in transfected cells 6fold, while that of the single isozymes each cause a 2fold increase in cAMP production, overview
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genetic disruption of adenylyl cyclase type 5 in mice leads to one-third longer live spans of the mutant mice compared to the wild-type mice, and protection from aging-induced, pressure overload-induced and catecholamine-induced stresses, AC5 KO mice are protected from the osteoporosis of aging, overview
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the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC8 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, isozyme AC8 KO mice display more dramatic impairments for the improvement in escape latency, saving time, and trial numbers needed to reach the escape latency criterion of 20 s compared to wild-type mice, phenotypes, overview
additional information
the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC8 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, isozyme AC8 KO mice display more dramatic impairments for the improvement in escape latency, saving time, and trial numbers needed to reach the escape latency criterion of 20 s compared to wild-type mice, phenotypes, overview
additional information
the basal phosphorylation levels of CREB are not changed in ACC slices from AC8 KO mice
additional information
the basal phosphorylation levels of CREB are not changed in ACC slices from AC8 KO mice
additional information
construction of AC8 knockout and AC1/8 double knockout mice, that exhibit reduced opiate, e.g. morphine, dependence on the basis of attenuated withdrawal, however, partially distinct withdrawal symptoms are affected in the two lines. The ability of chronic morphine to enhance the effect of forskolin on LC firing rates is completely abolished in AC8 and AC1/8 deficient mutants, morphine regulation of gene expression in locus coeruleus of AC8 KO mice, overview
additional information
construction of AC8 knockout and AC1/8 double knockout mice, that exhibit reduced opiate, e.g. morphine, dependence on the basis of attenuated withdrawal, however, partially distinct withdrawal symptoms are affected in the two lines. The ability of chronic morphine to enhance the effect of forskolin on LC firing rates is completely abolished in AC8 and AC1/8 deficient mutants, morphine regulation of gene expression in locus coeruleus of AC8 KO mice, overview
additional information
construction of male and female AC5 knockout mice. AC5KO mice show striking anxiolytic and antidepressant phenotypes on standard behavioral assays, phenotype, overview
additional information
construction of male and female AC5 knockout mice. AC5KO mice show striking anxiolytic and antidepressant phenotypes on standard behavioral assays, phenotype, overview
additional information
construction of male and female AC5 knockout mice. AC5KO mice show striking anxiolytic and antidepressant phenotypes on standard behavioral assays, phenotype, overview
additional information
construction of male and female AC1/8 double knockout mice and AC5 knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
construction of male and female AC1/8 double knockout mice and AC5 knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
construction of male and female AC1/8 double knockout mice and AC5 knockout mice. AC1/AC8 double knockout mice are hypoactive, exhibit diminished sucrose preference, and display alterations in neurotrophic signaling, generally consistent with a prodepressant phenotype. Neither line of mice display alterations in hippocampal cell proliferation, but altered BDNF signaling, phenotypes, overview
additional information
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AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
AC8 knockout mice show decreased Ca2+ -stimulated adenylate cyclase activity in the hippocampus, hypothalamus, thalamus, and brainstem, and exhibit little or no mossy fiber LTP, i.e. long-term potentiation, the long-lasting enhancement in communication between two neurons that results from stimulation. Short-term plasticity is also impaired in AC8 knockout mice. Double knockouts of both isozymes AC1 and AC8 also exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
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double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
double knockouts of both isozymes AC1 and AC8 exhibit a nearly complete loss of mossy fiber long-term potentiation
additional information
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AC5-/- mice, all of the major behavioral effects of morphine, including locomotor activation, analgesia, tolerance, reward, and physical dependence and withdrawal symptoms, are attenuated. Sniffing, ptosis, teeth chattering, and body tremor are markedly reduced, diarrhea and paw tremor are not significantly different, the number of jumps is dramatically increased. Behavioral effects of selective micro or delta opioid receptor agonists are lost, behavioral effects of selective kappa opioid receptor agonists are unaffected. Loss of AC5 does not alter expression levels of opioid receptor transcripts
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additional information
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Adcy1-/- mice lack the type 1 adenylyl cyclase, no compensatory changes in the levels of transcripts encoding the related type 8 adenylyl cyclase isoform in retinas of mice deficient in AC1, phenotype of AC1-deficient mice, overview. A dysfunction of Ca2+/CaM-stimulated adenylyl cyclase activity in Drd4-/-mouse retina appears to be due primarily to low levels of expression of the AC1 and not to changes in CaM expression
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additional information
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AC5-deficient (AC5-/-) mice, reduction of basal L-type Ca2+ currents is significantly less pronounced than in wild-type myocytes, isoproterenol effects on L-type Ca2+ currents are mitigated
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additional information
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generation of transgenic mice with disrupted AC5 or overexpressing AC5, the latter type shows less decreased heart rate in later phases within one parabola, the inverse heart rate is more variable in AC5 knockout mice and less variable in AC5 overexpressing mice compared to wild-type mice, overview
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additional information
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the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC1 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, phenotypes, overview
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additional information
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the Ca2+-stimulated enzyme activity is significantly reduced in the hippocampus of isozyme AC8 KO mice and totally lost in double-knockout AC1/AC8 mutant mice, isozyme AC8 KO mice display more dramatic impairments for the improvement in escape latency, saving time, and trial numbers needed to reach the escape latency criterion of 20 s compared to wild-type mice, phenotypes, overview
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additional information
from Ala232 N-terminal truncated mutant has much lower enzyme activity compared with the wild type, significant reduction in the apparent Vmax with no appreciable change in the apparent K' for ATP
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from Ala232 N-terminal truncated mutant has much lower enzyme activity compared with the wild type, significant reduction in the apparent Vmax with no appreciable change in the apparent K' for ATP
additional information
deletion in the shoulder domain of the holoenzyme, linking of the two adjoining Calpha positions of residues Ala93 and His103, which are 4.6 A apart, mutant enzyme is 7fold more active at pH 8.0 compared to the wild-type enzyme, and shows only a residual 3fold activation at pH 5.5. When the entire shoulder domain is deleted, residues Asp62 to Arg105, the phenotype is similar. This deletion joins the Calpha positions of residues Gly61 and Ala106, which are 6.4 A apart in the wild-type structure
additional information
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deletion in the shoulder domain of the holoenzyme, linking of the two adjoining Calpha positions of residues Ala93 and His103, which are 4.6 A apart, mutant enzyme is 7fold more active at pH 8.0 compared to the wild-type enzyme, and shows only a residual 3fold activation at pH 5.5. When the entire shoulder domain is deleted, residues Asp62 to Arg105, the phenotype is similar. This deletion joins the Calpha positions of residues Gly61 and Ala106, which are 6.4 A apart in the wild-type structure
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
mutation of N342 does not affect adenylyl cyclase activity in Rv1900c
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
additional information
-
by analyzing the genomic locus, Rv0890c can be expressed and purified. The NB-ARC domain binds ATP and ADP, but does not hydrolyze these nucleotides. Using systematic evolution of ligands by exponential enrichment (SELEX), DNA sequences are identified that bind to the HTH domain of Rv0890c. Uniquely, the HTH domain can also bind RNA
additional information
-
by analyzing the genomic locus, Rv0890c can be expressed and purified. The NB-ARC domain binds ATP and ADP, but does not hydrolyze these nucleotides. Using systematic evolution of ligands by exponential enrichment (SELEX), DNA sequences are identified that bind to the HTH domain of Rv0890c. Uniquely, the HTH domain can also bind RNA
-
additional information
-
from Ala232 N-terminal truncated mutant has much lower enzyme activity compared with the wild type, significant reduction in the apparent Vmax with no appreciable change in the apparent K' for ATP
-
additional information
-
deletion in the shoulder domain of the holoenzyme, linking of the two adjoining Calpha positions of residues Ala93 and His103, which are 4.6 A apart, mutant enzyme is 7fold more active at pH 8.0 compared to the wild-type enzyme, and shows only a residual 3fold activation at pH 5.5. When the entire shoulder domain is deleted, residues Asp62 to Arg105, the phenotype is similar. This deletion joins the Calpha positions of residues Gly61 and Ala106, which are 6.4 A apart in the wild-type structure
-
additional information
-
by analyzing the genomic locus, Rv0890c can be expressed and purified. The NB-ARC domain binds ATP and ADP, but does not hydrolyze these nucleotides. Using systematic evolution of ligands by exponential enrichment (SELEX), DNA sequences are identified that bind to the HTH domain of Rv0890c. Uniquely, the HTH domain can also bind RNA
-
additional information
-
disruption of the catalytic domain of CyaC significantly increases symbiotic competency with the symbiotic partner Blasia pusilla, whereas reduced infectivity is observed in a mutant disrupted close to the 6 N-terminus of CyaC. Total cellular cAMP levels are significantly reduced in both mutants
additional information
Q7A2D9
deletion of CyaC reduces cellular cAMP levels to 25% of wild-type, in the mutant cells cAMP levels are not lowered by light as in wild-type cells, but stay constant
additional information
Q8YVS0
deletion of CyaC reduces cellular cAMP levels to 25% of wild-type, in the mutant cells cAMP levels are not lowered by light as in wild-type cells, but stay constant
additional information
Q8YMH0
deletion of CyaC reduces cellular cAMP levels to 25% of wild-type, in the mutant cells cAMP levels are not lowered by light as in wild-type cells, but stay constant
additional information
Q7A2D9
engineering adenylate cyclase activated by near-infrared window light for mammalian optogenetic applications. The engineered NIRW-AC, designated IlaM5, has significantly higher activity at 37°C, is better expressed in mammalian cells, and can mediate cAMP-dependent photoactivation of gene expression in mammalian cells, in favorable contrast to the NIRW-ACs engineered earlier. The ilaM5 gene expressed from an AAV vector is delivered into the ventral basal thalamus region of the mouse brain resulting in the light-controlled suppression of the cAMP-dependent wave pattern of the sleeping brain known as spindle oscillations. Reversible spindle oscillation suppression is observed in sleeping mice exposed to light from an external light source. Cloning and method development, overview
additional information
-
generation of Plasmodium berghei parasites deficient in adenylyl cyclase alpha, ACa. The ACalpha-deficient sporozoites do not exocytose in response to migration through host cells and present more than 50% impaired hepatocyte infectivity in vivo compared to wild-type parasites, phenotype, overview
additional information
-
disruption of a class IIIb AC gene results in strong attenuation
additional information
AC7AC3 chimeric mutants, exchange of the putative transmembrane domains, M1 and M2 or of the N-terminal tail has no effect on the ethanol response of enzyme activity
additional information
AC7AC3 chimeric mutants, exchange of the putative transmembrane domains, M1 and M2 or of the N-terminal tail has no effect on the ethanol response of enzyme activity
additional information
AC7-AC2 chimeric mutants, regardless of the origin of the N-terminal tail, C1b, M1, and M2 domains, the ethanol response of the mutant is similar to that of the parent isoform of AC, from which the C1a and C2 domains are derived
additional information
AC7-AC2 chimeric mutants, regardless of the origin of the N-terminal tail, C1b, M1, and M2 domains, the ethanol response of the mutant is similar to that of the parent isoform of AC, from which the C1a and C2 domains are derived
additional information
-
genetic deletion of the second through fourth coding exons in Sacytm1Lex/Sacytm1Lex knockout mice, deficient in sperm soluble isozyme, results in a male sterile phenotype, the soluble isozymes from brain are not affected, overview
additional information
RNA interference knockdown of soluble adenylyl cyclase in mpkCCDc14 cells leads to a yield of about 60% knockdown of the predominant somatic soluble adenylyl cyclase isoforms of 50-53 kDa, also amiloride-sensitive Isc is inhibited to a comparable extent
additional information
construction and phenotypic characterization of a DELTAsac1 disruption strain, construction of single knockout mutants of the genes gsa and sac1, and DELTAgsa/DELTAsac1 double mutants and one DELTAgsa2/DELTAgsa3/DELTAsac1 triple mutant, phenotypes. While the single mutants show some reduction of fertility, double mutants DELTAgsa1/DELTAgsa2 and DELTAgsa1/DELTAgsa3 are completely sterile, overview
additional information
-
construction and phenotypic characterization of a DELTAsac1 disruption strain, construction of single knockout mutants of the genes gsa and sac1, and DELTAgsa/DELTAsac1 double mutants and one DELTAgsa2/DELTAgsa3/DELTAsac1 triple mutant, phenotypes. While the single mutants show some reduction of fertility, double mutants DELTAgsa1/DELTAgsa2 and DELTAgsa1/DELTAgsa3 are completely sterile, overview
additional information
-
strain lacking the Rv1264-like cyclase is unable to execute an apparently cAMP and acid pH-dependent differentiation pathway
additional information
-
truncated version of Cya1 consisting of amino acids 95 to 338, mutant with significant lower specific activity
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pH STABILITY
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
7 - 10
7 - 10
the purified recombinant retains more than 90% of residual activity after 10 h incubation at pH 7.0-10.0
7 - 10
the purified recombinant retains more than 90% of residual activity after 10 h incubation at pH 7.0-10.0
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TEMPERATURE STABILITY
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
-25
-40
28
-
plasma membrane isolated from glutamate/malate grown cells, no loss of activity after 10 min, plasma membrane isolated from lactic acid grown cells, little inactivation after 10 min
30
purified recombinant enzyme, loss of 90% activity within 12 h
35 - 45
purified recombinant enzyme, loss of all activity within 12 h
4 - 40
the purified recombinant enzyme retains more than 90% of residual activity after 12 h incubation
40
-
plasma membrane isolated from glutamate/malate grown cells, complete loss of activity after 3 min, plasma membrane isolated from lactic acid grown cells, complete inactivation after 4.5 min
45
4
purified recombinant enzyme, loss of 30% activity within 12 h
45
purified recombinant enzyme, loss of 40% activity within 12 h
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GENERAL STABILITY
ORGANISM
UNIPROT
LITERATURE
iodination, inactivation of free enzyme, enzyme-calmodulin complex stable 2 months
-
stabilized by ATP or at -20°C as an ammonium sulfate precipitate or in 50% glycerol
-
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STORAGE STABILITY
ORGANISM
UNIPROT
LITERATURE
-18C, membrane preparation, lyophilized, 1 week, 50% activity
-20°C, 50 mM Tris-HCl buffer, pH 8.5, 2 mM MgCl2, 10 mM NaCl, 35% glycerol
-80°C, 50 mM Tris-HCl, pH 8, 6 mM MgCl2, 0.1% Triton X-100, several weeks
-
-80°C, TrisHCl buffer, pH 8.3, KCl, dithiothreitol, several weeks
-
liquid N2, several months
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PURIFICATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
catalytic domain and the holoenzyme purified to homogeneity by Ni2+ affinity chromatography
full length Rv1264 protein purified to homogeneity
full length Rv1625c protein purified to homogeneity
glutathione Sepharose, column chromatography and Superdex G-25 gel filtration
-
glutathione-Sepharose 4B resin column chromatography, Q-Sepharose column chromatography, and Talon resin column chromatography
-
histidine-tagged auto-inhibitory domain Rv1264N, on nickel nitrilotriacetic acid/agarose column, to purity
Ni-NTA agarose column chromatography and Superose 12 gel filtration
partial
recombinant adenylyl cyclase
recombinant C-terminally His6-tagged fusions of IlaM5, IlaM4, IlaD9 and IlaC* from Escherichia coli by nickel affinity chromatography
Q7A2D9
recombinant His- and Spot-tagged LRR domain from Saccharomyces cerevisiae by affinnity chromatography
recombinant His-tagged adenylyl cyclases from Escherichia coli strain BL21(DE3) pLysS endo- by nickel affinity chrmatography, dialysis and gel filtration
-
recombinant His-tagged enzyme DdPAC from Escherichia coli strain LOBSTR by cobalt affinity chromatography, anion exchange chromatography, and dialysis
-
recombinant His-tagged enzyme from Escherichia coli strain BL21(DE3) by nickel affinity cjromatography
recombinant His-tagged enzyme from Escherichia coli strain BL21(DE3) Codon+ by nickel affinity chromatography and gel filtration, to homogeneity
recombinant His-tagged enzyme from Escherichia coli strain BL21-AI by nickel affinity chromatography
-
recombinant wild-type and mutant catalytic domain Cya2-446 from strain BL21(DE3) by nickel affinity chromatography
soluble isozyme
recombinant His-tagged enzyme from Escherichia coli strain BL21(DE3) by nickel affinity cjromatography
recombinant His-tagged enzyme from Escherichia coli strain BL21(DE3) by nickel affinity cjromatography
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CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
ACV fused with a GST tag and expressed in Escherichia coli, wild-type and mutant ACVIdeltaN enzymes expressed in Sf9 cells, COS-7 cells overexpressing ACVI, binding domain vector pGBKT7 together with pGADT7-beta1 or the activating vector pGADT7 together with pGBKT7-N-terminal region of ACV or ACVI co-transformed into AH109 cells
-
catalytic domain and the holoenzyme expressed in Escherichia coli BL21(DE3)[pREP4] as soluble proteins
chimeras inserted into the mammalian expression vector pCMV-SK, wild-type and chimeric mutants expressed in HEK-293 cells
class I AC gene, overexpression of wild-type and mutant catalytic domain, residues 2-446, i.e. Cya2-446, in strain BL21(DE3)
cloned into pET15b vector, recombinant plasmid isolated from Escherichia coli NovaBlue cells and introduced into Escherichia coli BL21(DE3) cells for protein expression
-
cloning of cDNA, expression in Sf9 cells, HEK293 and Xenopus laevis oocytes fails
cloning of cDNA, expression of synthetic AC gene PfAC526-884 in Sf9 cells
construction of a pcAmac3-HA expression vector, heterologous expression in flp-In-293 cells
Q1MU16
Escherichia coli BL21 (DE3) transformed with pET11D-AC5N1-215, AC5-myc and HA-Ric8a expressed in HEK-293T cells
expressed in Escherichia coli SG13009[pREP4] andM15[pREP4] cells
expressed in Escherichia coli strains BL21 (DE3) and BTH101, in Xenopus laevis oocytes, rat hippocampal pyramidal cells, and in the Drosophila melanogaster central nervous system
-
expressed in Sf9 insect cells
expression analysis of isozymes ACI-ACIX in wild-type and hypoxic retinas by real time PCR, overview
-
expression in Escherichia coli
expression in HEK 293 cells
expression in Sf9 cells
expression of C-terminal cytoplasmic domain of type II adenylyl cyclase in Escherichia coli
-
expression of C-terminal domain as GST-fusion protein in Escherichia coli
expression of cyaB1-1-859 AC holoenzyme and catalytic domain cyaB1-595-859 in Escherichia coli
expression of cytosolic domain of type V adenylyl cyclase in Escherichia coli
-
expression of different recombinant forms of adenylate cyclase toxin, insertion mutant CyaA, fully functional CyaA, CyaA* lacking adenylate cyclase enzymatic activity CyaA*, and non-acylated forms of the two latter toxins, proCyaA and proCyaA*
expression of fluorescent EGFP-tagged isozyme AC5, and of the fluorescence-tagged chimeric mutant dimer of AC2/AC5 in HEK-293-F cells, subcellular distribution, overview
expression of fluorescent Luc-tagged isozyme AC2, and of the fluorescence-tagged chimeric mutant dimer of AC2/AC5 in HEK-293-F cells, subcellular distribution, overview
expression of full length and C-terminal truncated sAC in HEK293 cells
expression of full length and truncated sAC in HEK293 cells
expression of His-tagged truncated cyclase domain in Escherichia coli C41. The mutant enzyme E497K/C566D is expressed the N-terminal YFP-tagged constructs in oocytes
expression of isozyme ACVI in Spodoptera frugiperda Sf9 cell membranes, with a combination of four recombinant baculoviruses individually encoding the dopamine D1 receptor, G-protein alphaS-subunit, G-protein beta1gamma2 subunit dimer, and adenylyl cyclase type VI, ACVI. The recovered budded virus fraction produces cAMP in response to the stimulation with dopamine. Co-expression of all three G-protein subunits inaddition to receptor and ACVI led to amaximal response. Budded virusses co-expressingthel proteins also respond to dopamine agonists fenoldopam and SKF38393 and the antagonist flupenthixol, overview
expression of isozyme ACVI with an AU1 tag, a 6-amino acid epitope DTYRY, in Rattus norvegicus myocytes using an adenoviral vector leading to increased phosphorylation of phospholamban independently of beta-adrenergic receptor stimulation, and to increased Akt activity, 5fold, and phosphorylation at both the Ser473 and Thr308 sites, but does not change the levels of Akt protein, phosphorylation of GSK alpha- and beta-isoforms is also increased by the gene transfer, overview
-
expression of maltose binding protein-cyaC fusion protein in Escherichia coli
expression of Mus musculus isozyme ACVI with an AU1 tag, a 6-amino acid epitope DTYRY, in rat myocytes using an adenoviral vector leads to increases phosphorylation of phospholamban independently of beta-adrenergic receptor stimulation
-
expression of native and truncated CyaB1 as CyaB1-maltose binding protein fusion protein
-
expression of splice variant 3 in Xenopus laevis, expression of splice variants 1 and 3 in Dictyostelium
expression of the N-terminally His-tagged catalytic domain of CyaC
expression of transmembrane isozymes in HEK293T cells, expression of GST-tagged soluble isozyme
expression of transmembrane isozymes in HEK293T cells, expression of His-tagged soluble isozyme
-
gene Adcy1, DNA and amino acid sequence determination and analysis, expression analysis, genotyping
-
gene adcy10, DNA and amino acid sequence determination and analysis, sequence comparisons and phylogenetic analysis, identification of rtsAC splice variants, RT-PCR enzyme expression analysis, recombinant expression of N-terminally His6-tagged enzyme in Escherichia coli strain BL21-AI
-
gene ADCY9, For Myc-AC9-VN and HA-AC9-VC, the N-terminal half of Venus (VN) and the C-terminal half of Venus (VC) are cloned using polymerase chain reaction (PCR) in frame with the C-terminus of full-length AC9, separated by a sequence encoding a 12- and 19-amino-acid linker, respectively. Additional AC9-VN and AC9-VC constructs that lack an N-terminal tag are generated and consisted of a C-terminal 7-amino-acid linker (AAAGGGS) followed by VN or VC tags. Recombinant expression in HEK-293 cells and COS-7 cells, recombinant expression in Spodoptera frugiperda Sf9 cell membranes
gene cyaA, DNA and amino acid sequence determination and analysis, genotyping and phylogenetic analysis of strains RB50 and 253, overview
-
gene CYR1, construction of an expression vector for the Cyr1p-LRR domain containing residues from position 435 to the PP2C domain. The construct contains 14 repeats of the LRR domain and is expressed in Saccharomyces cerevisiae, recombinant expression of His- and Spot-tagged LRR domain in Saccharomyces cerevisiae
gene ilaM5, recombinant expression of C-terminally His6-tagged fusions of IlaM5, IlaM4, IlaD9 and IlaC* in Escherichia coli, recombinant expression of C-terminally His6-tagged IlaM5 and IlaC* proteins in human embryonic kidney HEK293 cells
Q7A2D9
gene TTD1, recombinant expression in and complementation of AC-deleted Escherichia coli strain SP850
-
gene TTD2, recombinant expression in and complementation of AC-deleted Escherichia coli strain SP850
-
h5-HT6 pHTop CHODUKX-A2 cells transiently transfected with human Golf, Gs proteins and rat AC2, AC5 full-length isoforms
-
HEK293 cells transiently transfected with pcDNA3 containing either GFP or Flag-tagged AC1, AC2 and AC5 or AC6 cDNA
-
locus CLV30_10882, sequence comparisons, recombinant expression of His-tagged enzyme in Escherichia coli strain BL21(DE3)
locus NI17_09695, sequence comparisons, recombinant expression of His-tagged enzyme in Escherichia coli strain BL21(DE3)
overexpression of AC5 and AC6 in CHO cells co-transfected with A2bR in pCB6 expression vector along with AC5 and AC6 expression vectors
-
overexpression of nine membrane-bound isozymes in COS7 cells in absence of the D1 receptor
-
overexpression of Rv1625c in Escherichia coli and expressed in mammalian cells
overexpression of the histidine-tagged auto-inhibitory domain Rv1264N in Escherichia coli BL21(DE3)[pREP4] cells
overexpression of untagged AC8 and C-terminally HA-tagged AC8 in HEK293 cells, co-expression of HA-tagged AC8, myc-tagged Orai1 and untagged STIM1 in membranes, and co-expression of CFP-tagged AC8, YFP-tagged STIM1 and myc-tagged Orai1 with co-localization at the plasma membrane
polymorphism genotyping, and ADRB2 and ADCY6 gene interaction. The effect of ADRB2 on adhesion of erythrocytes in the sickle cell disease is different depending on the genotype of ADCY6. Sickle red cells from patients who were homozygous for either the G allele at single nucleotide polymorphism rs3730070 of ADCY6 demonstrate significantly increased adhesion to laminin compared to red cells from control patients, overview
-
recombinant expression of C-terminally His-tagged enzyme DdPAC in Escherichia coli strain LOBSTR
-
recombinant expression of C-terminally His-tagged enzyme in Escherichia coli strain BL21(DE3) Codon+
recombinant expression of engineered enzyme constructs in stable MVD7 cell lines and in HEK-293T I/17 cells
A7BT71
stable recombinant overexpression of isozyme AC6 in HEK-293 cells, recombinant expression of N-terminally FLAG-tagged AC isoform 6 in HEK-293 cells
subcloned into pQE30, fitted with an N-terminal MRGSH6GS dodecapeptide affinity tag and expressed in Escherichia coli M15 [pREP4] cells
-
the ADCY10 gene is located in the region linked to spinal bone mineral density
-
the putative catalytic domain (amino acids 217-463) as an N-terminal hexahistidine fusion is expressed in Escherichia coli M15[pREP4] cells
-
the rv0891c-rv0890c genes are fused and encode a protein with all four domains present in a single polypeptide, this fusion is a result of the absence of the T residue in the TGA codon of rv0891c thereby removing a stop codon and allowing the remaining basepairs to code for a Glu residue. Recombinant expression of His-tagged adenylyl cyclase in Escherichia coli strain BL21(DE3) pLysS endo- under control of the SigA promoter, genetic structure and expression analysis
-
the testis isozyme is located in the Sacytm1Lex locus, sAC transcripts in brain use an alternate start site than the testis isozyme transcripts
-
transfection of Rattus norvegicus primary culutres of dentate granule cells
transient expression of fluorescent EGFP-tagged AC6 truncation mutants, expression of isozyme AC6 in COS-7 cells, expressing caveolin-1, and in HEK-293 cells or cardiac fibroblasts isolated from caveolin-1 knock-out mice, localization of AC6 in lipid rafts in all cell types, association via the AC6 C-terminal domains, expression analysis, overview
-
transient expression of tagged isozyme AC3 in HEK-PR1 cells, AC6 forms complexes with the IP3 R2 receptor
chimeras inserted into the mammalian expression vector pCMV-SK, wild-type and chimeric mutants expressed in HEK-293 cells
chimeras inserted into the mammalian expression vector pCMV-SK, wild-type and chimeric mutants expressed in HEK-293 cells
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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
addition of GTP/Mn2+ reveals the cyclase domain to be constitutively active
in SK-N-SH human neuroblastoma cells, morphine significantly increases RNA transcript and protein levels of type I adenylate cyclase
-
isoform AC6 expression is stimulated by forskolin and isoproterenol (0.01 mM)
-
addition of GTP/Mn2+ reveals the cyclase domain to be constitutively active
addition of GTP/Mn2+ reveals the cyclase domain to be constitutively active
-
-
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RENATURED/Commentary
ORGANISM
UNIPROT
LITERATURE
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APPLICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
analysis
drug development
medicine
molecular biology
pharmacology
additional information
analysis
-
technical problems of AC detection, some of which caused by poor quality-control of commercially supplied antibodies. Intracellular targeting of ACs may be isoform-specific and also dependent on the cellular context of expression
analysis
-
technical problems of AC detection, some of which caused by poor quality-control of commercially supplied antibodies. Intracellular targeting of ACs may be isoform-specific and also dependent on the cellular context of expression
analysis
-
technical problems of AC detection, some of which caused by poor quality-control of commercially supplied antibodies. Intracellular targeting of ACs may be isoform-specific and also dependent on the cellular context of expression
analysis
-
technical problems of AC detection, some of which caused by poor quality-control of commercially supplied antibodies. Intracellular targeting of ACs may be isoform-specific and also dependent on the cellular context of expression
analysis
the enzyme activity is useful as a marker for determination of G-protein-coupled receptor function mediating adenylyl cylcase activation by extracellular baculovirus particles, usage of this budded virus display system to detect G-protein-coupled receptor signaling, method development, overview
analysis
development of a fluorescence resonance energy transfer (FRET) sensor that functions both as a soluble cyclase and a reporter of complementation within the catalytic domain. There is a strong linear correlation between catalytic domain complementation and cyclase activity upon stimulation with forskolin and the Galphas subunit. The sensor is functional in live cells
analysis
-
technical problems of AC detection, some of which caused by poor quality-control of commercially supplied antibodies. Intracellular targeting of ACs may be isoform-specific and also dependent on the cellular context of expression
-
drug development
-
CyaA substantially contributes to the pathogenesis of whooping cough, catalytic site of CyaA possesses substantial conformational freedom to accommodate structurally diverse ligands, certain ligands bind to CyaA even in the absence of calmodulin, facilitating future inhibitor design
drug development
-
stable AC2-expressing CHODUKX cell line in which the generation of high expressing GPCR receptor/AC2 lines can retain their functional responsiveness and can provide pharmacological drug comparisons between the same host line for screening purposes and measurement of multiple cellular parameters
drug development
-
AC1 is a potential drug target site to improve long-term remote memor
drug development
due to its significance in heart disease and dyskinesia, human isozyme AC5 is an important therapeutic target
medicine
-
induction of cardiac myocyte apoptosis by high beta-adrenergic receptor stimulation is effectively prevented by type 5 adenylyl cyclase inhibitors. Inhibition of adrenergic signaling at the level of the type 5 adenylyl cyclase isoform by P-site inhibitors may serve as an effective method to prevent cardiac myocyte apoptosis induced by excessive adrenergic stimulation without deleterious effect on cardiac myocyte contraction
medicine
-
sAC plays a critical role in cAMP signaling in spermatozoa, defective cAMP production prevents engagement of multiple components of capacitation resulting in male infertility. sAC and cAMP coordinate cellular energy balance in wild-type sperm. sAC appears to be a promising target for the development of male contraceptives
medicine
-
AC5 is the major AC isoform mediating acute beta-adrenergic stimulation, AC5 plays a major role in L-type Ca2+ currents activation
medicine
-
AC1 and AC8 involved in long-term memory and in N-methyl-D-aspartate-dependent long-term potentiation, AC1 and AC8 are not required for acute pain response. AC1 is the major Ca2+ sensor for N-methyl-D-aspartate receptor activation and excitotoxicity
medicine
-
sAC and the vacuolar proton pumping ATPase have a close association, may be part of a protein complex that is involved in regulating renal distal proton secretion
medicine
-
sAC and the vacuolar proton pumping ATPase have a close association, may be part of a protein complex that is involved in regulating renal distal proton secretion
medicine
-
AC6, but not AC5, mRNA is decreased in rats with cardiac hypertrophy after myocardial infarction, overexpression of AC6 in cardiac fibroblasts impairs collagen synthesis in response to serum or other activators
medicine
-
overexpression of AC6 prevents development of cardiac hypertrophy, restores normal cardiac function, improves mortality rate, and contractile function. Overexpression of AC5 also restores cAMP signaling and contractile deficits, but cardiac hypertrophy still develops. Decreased AC5 expression does not diminish cardiac funcition, may be beneficial in mice experiencing artificial pressure overload
medicine
-
overexpression of AC6 or drug-stimulated cAMP accumulation in WI-38 lung fibroblast attenuates fibrosis
medicine
-
involved in mediating opioid actions, AC5 is essential for micro, and to a lesser extent, delta, opioid receptor signaling in striatum
medicine
-
A2bR mediates signaling through AC-6 isoform, therapeutic implications for intestinal inflammation or diarrhea wherein A2bR is upregulated
medicine
-
A2bR mediates signaling through AC-6 isoform, therapeutic implications for intestinal inflammation or diarrhea wherein A2bR is upregulated
medicine
-
cumulus cells possess multiple active isoforms of adenylyl cyclase, each isoform may have a specific role at a specific time during oocyte growth and maturation
medicine
-
inhibition of adenylyl cyclase type 5 is a strategy to treat heart failure
medicine
-
isoform ACbeta represents a potential target for development of safe and effective antimalarial therapeutics
medicine
isoform Adcy1 catalytic activity can be delicately adjusted by mediating calmodulin activation of Adcy1 by reversible Met oxidation in calmodulin
medicine
-
involved in mediating opioid actions, AC5 is essential for micro, and to a lesser extent, delta, opioid receptor signaling in striatum
-
medicine
-
AC5 is the major AC isoform mediating acute beta-adrenergic stimulation, AC5 plays a major role in L-type Ca2+ currents activation
-
molecular biology
the enzyme is a favorable optogenetic tools for non-invasive, cell-selective, and spatio-temporally precise modulation of cAMP/cGMP with light. The rhodopsin domain from Catenaria is more photostable than that from Blastocladiella, and the signaling state persists longer, both of which are highly desirable traits for optogenetic applications
molecular biology
-
the enzyme is a favorable optogenetic tools for non-invasive, cell-selective, and spatio-temporally precise modulation of cAMP/cGMP with light. The rhodopsin domain from Catenaria is more photostable than that from Blastocladiella, and the signaling state persists longer, both of which are highly desirable traits for optogenetic applications
-
pharmacology
-
activation of cardiac adenylyl cyclase isozyme ACVI expression increases the function of the failing ischemic heart in mice, overview. Increased left ventricular ACVI content also markedly reduces mortality and increases left ventricular function after acute myocardial infarction in mice
pharmacology
pharmacological approaches do not allow cell specific manipulation of cyclic nucleotides in tissue and lack precision in space and time, limitations that can be overcome using the light-activated enzyme
pharmacology
-
pharmacological approaches do not allow cell specific manipulation of cyclic nucleotides in tissue and lack precision in space and time, limitations that can be overcome using the light-activated enzyme
-
additional information
-
activation of the HCO3-/sAC transduction pathway enhances both cftr gene and CFTR protein expression and appears to be a physiological mechanism whereby the cell adapts to variations in extracellular HCO3- concentration
additional information
Q1MU16
shares high sequence similarity (approximately 62%) with the Drosophila AC39E, enzyme serves in biogenic amine signal transduction cascades and in higher brain functions that contribute to learning and memory of the bee
additional information
-
shares high sequence similarity (approximately 62%) with the Drosophila AC39E, enzyme serves in biogenic amine signal transduction cascades and in higher brain functions that contribute to learning and memory of the bee
additional information
-
AC8 acts as a low-pass filter for high-frequency Ca2+ events, enhancing the regulatory options available to this signalling pathway
additional information
-
Rv1264 plays a role in mycobacterial survival in the acidic environment of the pahgolysosome
additional information
-
restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
-
restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
-
restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
-
restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
-
Ca2+-stimulated AC regulates If via cAMP, modulation of the If pacemaker current
additional information
-
sAC is localized to motile airway cilia and it contributes to the regulation of human airway ciliary beat frequency in conditions of changing intracellular CO2/HCO3- via production of cAMP
additional information
-
endothelin-1 deficiency increases inner medullary collecting duct AC5/6 content, that may synergize with acute endothelin-1 inhibition of vasopressin-stimulated cAMP accumulation
additional information
interaction between the N-terminus of AC5 and the guanine nucleotide exchange factor Ric8a provides a pathway to fine-tune AC5 activity via a Galphai mediated pathway
additional information
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overexpression of AC1 in forebrain enhances long-term potentiation
additional information
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essential role of Ca2+/calmodulin-regulated ACs in learning and memory
additional information
Rv2212 gene has a domain composition identical to that of the AC isoform Rv1264, limited similarity of the N-termini, N-terminal domain of Rv2212 is not autoinhibitory as in Rv1264
additional information
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Rv2212 gene has a domain composition identical to that of the AC isoform Rv1264, limited similarity of the N-termini, N-terminal domain of Rv2212 is not autoinhibitory as in Rv1264
additional information
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compartmentalization of cAMP signalling, cAMP levels change in discrete domains of the cell with discrete local consequences
additional information
Q7CH76
class IV AC fold is distinct from the previously described folds for class II and class III ACs
additional information
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class IV AC fold is distinct from the previously described folds for class II and class III ACs
additional information
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isoform-selective signaling complexes likely contribute to various functional consequences of cAMP elevation in vascular smooth muscle cells. AC1 isoform contributes to modulation of extracellular signal-regulated kinase signaling, proliferation, and control of cell division, whereas AC6, at least partly because of uncoupling of cAMP synthesis from cAMP breakdown, results in sustained cAMP accumulation, vasodilator-stimulated phosphoprotein phosphorylation, and control of cytoskeletal rearrangements that contribute to vascular arborization
additional information
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both sAC and tmACs participate in the sperm acrosome reaction and sperm motility
additional information
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ACA has the same architecture as mammalian membrane-bound ACs, is essential for reacting to and production of cAMP. ACG is essential for germination. ACB is required for terminal maturation of spores
additional information
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ACIII is a marker for primary cilia throughout many regions of the adult mouse brain
additional information
Q7A2D9
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q8YVS0
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q8YMH0
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q7A2D9
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q8YVS0
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q8YMH0
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
Q7A2D9
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
Q8YVS0
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
Q8YMH0
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
-
ACT enhances the adhesive functions of filamentous haemagglutinin and modifies the performance of the filamentous haemagglutinin heparin-inhibitable carbohydrate binding site
additional information
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membrane transitions in cAMP strengthen the endothelial cell barrier, whereas the production of cAMP by soluble AC within the cytosol away from the membrane disrupts the endothelial cell barrier
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv1120c is a pseudogene in Mycobacterium tuberculosis
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
Rv1625c has the highest sequence similarity with the mammalian enzymes
additional information
A0A068MZJ9
construction of a fusion between Deinococcus radiodurans bacteriophytochrome linked to Synechocystis sp. guanylate/adenylate cyclase. The construct shows low dark-state activity and high dynamic range that outperforms previous optogenetic tools in vitro
additional information
Q7A2D9
robustness of principles of homodimeric bacteriophytochrome engineering, describes a NIRW-AC suitable for mammalian optogenetic applications, and demonstrates feasibility of controlling brain activity via NIRW-ACs using transcranial irradiation
additional information
-
Rv2212 gene has a domain composition identical to that of the AC isoform Rv1264, limited similarity of the N-termini, N-terminal domain of Rv2212 is not autoinhibitory as in Rv1264
-
additional information
-
Rv1647 adenylyl cyclase has a cyclase domain that is more closely related to fungal and protist cyclases
-
additional information
-
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
-
additional information
-
Rv1625c has the highest sequence similarity with the mammalian enzymes
-
additional information
-
ACT enhances the adhesive functions of filamentous haemagglutinin and modifies the performance of the filamentous haemagglutinin heparin-inhibitable carbohydrate binding site
-
additional information
-
ACIII is a marker for primary cilia throughout many regions of the adult mouse brain
-
EXTERNAL LINKS (specific for EC-Number 4.6.1.1)
Transporter Classification Database (TCDB): 8.A.85.1.4
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Release 2026.1 (March 2026)
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