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2 GTP
c-diGMP + 2 diphosphate
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adenyloimidodiphosphate
?
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adenylomethyloendiphosphate
?
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?
ATP
3',5'-cAMP + diphosphate
ATP
3',5'-cyclic AMP + diphosphate
ATP
3',5'-cyclic-AMP + diphosphate
dATP
deoxy-cAMP + diphosphate
-
-
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?
deoxy-cAMP + diphosphate
ATP
-
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r
GTP
3',5'-cGMP + diphosphate
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GTP
3',5'-cyclic-GMP + diphosphate
Q7CH76
class IV adenylyl cyclase also functions as guanylyl cyclase with about 20% efficiency
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additional information
?
-
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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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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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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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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ATP
3',5'-cAMP + diphosphate
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?
ATP
3',5'-cAMP + diphosphate
-
catalytic heterodimer VC1-IIC2
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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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ATP
3',5'-cAMP + diphosphate
-
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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ATP
3',5'-cAMP + diphosphate
-
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r
ATP
3',5'-cAMP + diphosphate
-
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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ATP
3',5'-cAMP + diphosphate
-
-
664044, 678381, 679107, 679659, 679862, 680828, 681009, 681169, 682112, 682285, 682958 -
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?
ATP
3',5'-cAMP + diphosphate
-
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?
ATP
3',5'-cAMP + diphosphate
-
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r
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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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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ATP
3',5'-cAMP + diphosphate
-
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ATP
3',5'-cAMP + diphosphate
-
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?
ATP
3',5'-cAMP + diphosphate
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 -
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?
ATP
3',5'-cAMP + diphosphate
-
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?
ATP
3',5'-cAMP + diphosphate
ATP substrate affinity is low
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ATP
3',5'-cAMP + diphosphate
-
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
O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35 -
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-
?
ATP
3',5'-cAMP + diphosphate
ATP substrate affinity is low
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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
Nocardia erythropolis
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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
in CyaB1 only GAFB binds cAMP
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?
ATP
3',5'-cAMP + diphosphate
in CyaB2 both GAFA and GAFB are cAMP receptors
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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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ATP
3',5'-cAMP + diphosphate
-
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?
ATP
3',5'-cAMP + diphosphate
-
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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ATP
3',5'-cAMP + diphosphate
-
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ATP
3',5'-cAMP + diphosphate
-
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
-
catalytic heterodimer VC1-IIC2
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ATP
3',5'-cAMP + diphosphate
-
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
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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
squirrel
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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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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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?
ATP
3',5'-cAMP + diphosphate
-
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?
ATP
3',5'-cAMP + 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
-
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
adenylyl cyclase activity results from the point mutations E497K/C566D in guanylyl cyclase
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?
ATP
3',5'-cyclic AMP + diphosphate
adenylyl cyclase activity results from the point mutations E497K/C566D in guanylyl cyclase
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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
-
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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
adenylyl cyclase also displays ion channel properties
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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
adenylyl cyclase also displays ion channel properties
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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
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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
adenylyl cyclase also displays ion channel properties
-
?
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
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?
ATP
3',5'-cyclic-AMP + diphosphate
-
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
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
-
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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?
ATP
3',5'-cyclic-AMP + diphosphate
-
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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?
ATP
3',5'-cyclic-AMP + diphosphate
-
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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ATP
3',5'-cyclic-AMP + diphosphate
-
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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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
-
the enzyme is involved in regulation of presynaptic terminal excitability
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?
ATP
3',5'-cyclic-AMP + diphosphate
-
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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?
ATP
3',5'-cyclic-AMP + diphosphate
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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?
ATP
3',5'-cyclic-AMP + diphosphate
-
the enzyme acts as a photoreceptor for step-up photophobic response
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ATP
3',5'-cyclic-AMP + diphosphate
-
-
691237, 691562, 691574, 691711, 691723, 693757, 693772, 694258, 694376, 695074, 695078, 707396, 707490, 708403, 709018, 709679, 709693, 713708 -
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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
-
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
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
-
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
-
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
-
the enzyme is involved in cAMP signaling and cAMP/PKA-mediated growth inhibition
cAMP activates protein kinase A
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?
ATP
3',5'-cyclic-AMP + diphosphate
the reaction is part of the cAMP signaling pathways, overview
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?
ATP
3',5'-cyclic-AMP + diphosphate
the reaction is part of the cAMP signaling pathways, overview
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
-
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
-
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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ATP
3',5'-cyclic-AMP + diphosphate
-
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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?
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
-
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
-
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
-
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
-
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
-
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
-
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
-
enzyme regulation in cAMP signalling, overview
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
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
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
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
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
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
the cardiac-specific isozyme AC5 plays an important role in regualting heart rate during parabolic flights, overview
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
type 1 adenylyl cyclase is essential for maintenance of remote contextual fear memory
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
the C1 and C2 domains form a single ATP-binding at their interface
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
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
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
enzyme regulation in cAMP signalling, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
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
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
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
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
regulation of isozymes in the plasma membrane, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
cAMP signaling pathway mediates the activation of exocytosis in sporozoites, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
690360, 690680, 691561, 691562, 692562, 693180, 693436, 693560, 693763, 693803, 693830, 693847, 694363, 694374, 694823, 707801, 707947, 710009, 716279 -
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?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
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
-
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
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
-
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
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
-
soluble isozymes sAC play a unique function in male germ cells, overview
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
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
-
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
-
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
-
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
-
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
-
-
-
-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
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?
ATP
3',5'-cyclic-AMP + diphosphate
-
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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?
ATP
3',5'-cyclic-AMP + diphosphate
SAC1 acts downstream of heterotrimeric G protein GSA3, parallel to a GSA1-GSA2-mediated signaling pathway
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-
?
ATP
3',5'-cyclic-AMP + diphosphate
-
-
-
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?
ATP
3',5'-cyclic-AMP + diphosphate
Q7CH76
-
-
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?
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
-
-
-
-
r
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
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-
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?
ATP
cAMP + diphosphate
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?
ATP
cAMP + diphosphate
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?
MgATP2-
?
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?
MgATP2-
?
-
at pH 7.5
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?
MnATP2-
?
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?
additional information
?
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-
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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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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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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-
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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-
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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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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-
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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-
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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-
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
?
-
structure-function relationship, overview
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?
additional information
?
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-
structure-function relationship, overview
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?
additional information
?
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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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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
?
-
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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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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-
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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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
?
-
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
?
-
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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-
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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-
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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-
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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-
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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-
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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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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-
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
-
-
?
additional information
?
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-
AC1 is expressed throughout the trigeminal pathway
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?
additional information
?
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-
adenylyl cyclase-5 activity in the nucleus accumbens regulates anxiety-related behavior, overview
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?
additional information
?
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-
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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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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?
additional information
?
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-
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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-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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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-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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
?
-
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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-
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
?
-
-
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
?
-
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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-
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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-
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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-
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
?
-
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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-
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
-
-
?
additional information
?
-
-
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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-
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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-
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
?
-
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
?
-
-
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
?
-
soluble adenylyl cyclase inhibition blocks ATPase activity without affecting surface expression of the Na+ pump
-
-
?
additional information
?
-
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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-
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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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
?
-
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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-
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
-
-
?
additional information
?
-
Q7CH76
class IV adenylyl cyclase also functions as guanylyl cyclase
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?
additional information
?
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-
class IV adenylyl cyclase also functions as guanylyl cyclase
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?
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ATP
3',5'-cAMP + diphosphate
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ATP
3',5'-cyclic AMP + diphosphate
ATP
3',5'-cyclic-AMP + diphosphate
additional information
?
-
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
-
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
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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
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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
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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
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ATP
3',5'-cyclic-AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
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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
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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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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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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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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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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ATP
3',5'-cyclic-AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
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the enzyme is involved in regulation of presynaptic terminal excitability
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ATP
3',5'-cyclic-AMP + diphosphate
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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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ATP
3',5'-cyclic-AMP + diphosphate
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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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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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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
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
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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
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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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the enzyme is involved in cAMP signaling and cAMP/PKA-mediated growth inhibition
cAMP activates protein kinase A
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ATP
3',5'-cyclic-AMP + diphosphate
the reaction is part of the cAMP signaling pathways, overview
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ATP
3',5'-cyclic-AMP + diphosphate
the reaction is part of the cAMP signaling pathways, overview
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
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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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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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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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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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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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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
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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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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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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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enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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
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
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
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
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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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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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enzyme regulation in cAMP signalling, overview
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ATP
3',5'-cyclic-AMP + diphosphate
isozyme AC8 is required for the hippocampus-dependent working/episodic-like memory, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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
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ATP
3',5'-cyclic-AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
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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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regulation of isozymes in the plasma membrane, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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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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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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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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ATP
3',5'-cyclic-AMP + diphosphate
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ATP
3',5'-cyclic-AMP + diphosphate
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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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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
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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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
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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soluble isozymes sAC play a unique function in male germ cells, overview
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ATP
3',5'-cyclic-AMP + diphosphate
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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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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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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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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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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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ATP
3',5'-cyclic-AMP + diphosphate
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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
SAC1 acts downstream of heterotrimeric G protein GSA3, parallel to a GSA1-GSA2-mediated signaling pathway
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MgATP2-
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at pH 7.5
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MnATP2-
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additional information
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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AC1 is expressed throughout the trigeminal pathway
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additional information
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adenylyl cyclase-5 activity in the nucleus accumbens regulates anxiety-related behavior, overview
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additional information
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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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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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cyclase 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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cyclases 2 and 5 constitutively form a functional heterodimeric complex in HEK293 cells, overview
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additional information
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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-
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
?
-
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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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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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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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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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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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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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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soluble adenylyl cyclase inhibition blocks ATPase activity without affecting surface expression of the Na+ pump
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?
additional information
?
-
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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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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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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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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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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(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
1-(bromo(1-naphthyl)methyl)naphthalene
-
17beta-estra-1(10),2,4-triene-2,3,17-triol
-
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)-ADP
slight competitive inhibition
2'(3')-O-(N-methylanthraniloyl)-AMP
slight competitive inhibition
2'(3')-O-(N-methylanthraniloyl)-ATP
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
-
-
2'(3')-O-(N-methylanthraniloyl)-CTP
-
-
2'(3')-O-(N-methylanthraniloyl)-GTP
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
-
-
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-(N-methylanthraniloyl)-ITP
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
-
-
2'(3')-O-(N-methylanthraniloyl)-UTP
-
-
2',3'-bis[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
2',3'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
2',3'-isopropylidene adenosine
-
-
2',3'-O-(2,4,6-trinitrophenyl)-ADP
2',3'-O-(2,4,6-trinitrophenyl)-AMP
2',3'-O-(2,4,6-trinitrophenyl)-ATP
2',3'-O-(2,4,6-trinitrophenyl)-CTP
2',3'-O-(2,4,6-trinitrophenyl)-GDP
2',3'-O-(2,4,6-trinitrophenyl)-GTP
2',3'-O-(2,4,6-trinitrophenyl)-UTP
2',3'-O-(N-anthraniloyl)-ADP
-
-
2',3'-O-(N-anthraniloyl)-ATP
-
-
2',3'-O-(N-anthraniloyl)-IMP
-
-
2',3'-O-(N-methylanthraniloyl)-ADP
-
-
2',3'-O-(N-methylanthraniloyl)-ATP
-
-
2',3'-O-(N-methylanthraniloyl)-CDP
-
-
2',3'-O-(N-methylanthraniloyl)-CTP
-
-
2',3'-O-(N-methylanthraniloyl)-GTP
-
-
2',3'-O-(N-methylanthraniloyl)-GTPgammaS
-
potent inhibitor of isoform AC5
2',3'-O-(N-methylanthraniloyl)-IDP
-
-
2',3'-O-(N-methylanthraniloyl)-IMP
-
-
2',3'-O-(N-methylanthraniloyl)-ITP
-
-
2',3'-O-(N-methylanthraniloyl)-ITPgammaS
-
potent inhibitor of isoform AC5
2',3'-O-(N-methylanthraniloyl)-UDP
-
-
2',3'-O-(N-methylanthraniloyl)-UTP
-
-
2',3'-O-(N-methylanthraniloyl)-XTP
-
-
2',3'-O-bis(5-acetamidoanthraniloyl)-ATP
-
-
2',3'-O-bis(5-bromoanthraniloyl)-ADP
-
-
2',3'-O-bis(5-bromoanthraniloyl)-ATP
-
-
2',3'-O-bis(5-bromoanthraniloyl)-ITP
-
-
2',3'-O-bis(5-chloroanthraniloyl)-ATP
-
-
2',3'-O-bis(5-chloroanthraniloyl)-ITP
-
-
2',3'-O-bis(5-methylanthraniloyl)-ADP
-
-
2',3'-O-bis(5-methylanthraniloyl)-ATP
-
-
2',3'-O-bis(5-methylanthraniloyl)-CTP
-
-
2',3'-O-bis(5-methylanthraniloyl)-IDP
-
-
2',3'-O-bis(5-methylanthraniloyl)-IMP
-
-
2',3'-O-bis(5-methylanthraniloyl)-ITP
-
-
2',3'-O-bis(5-propylanthraniloyl)-ATP
-
-
2',3'-O-bis(5-propylanthraniloyl)-ITP
-
-
2',3'-O-bis-anthraniloyl-IMP
-
-
2',3'-O-isopropylidene adenosine
-
specifically inhibits ACA in intact cells, without affecting ACB or ACG
2',5'-dd-3'-ATP
-
most potent inhibitor
2',5'-dideoxy-3'-adenosine triphosphate
IC50 of about 730 nM
2',5'-dideoxyadenosine 3'-monophosphate
-
-
2',5'-dideoxyadenosine-3'-triphosphate
-
-
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'-deoxy-3'-adenosine monophosphate
IC50 of about 50 microM
2'-deoxy-3'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
-
2'-deoxy-3'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
-
2'-deoxyadenosine 3'-monophosphate
0.1 mM, 50% inhibition
2'-methylanthraniloyl-3'-d-ATP
-
-
2'-O-(N-methylanthraniloyl)-3'-deoxy-GTP
-
determination of Ki values under various experimental conditions
2,3,6,23-tetrahydroxyurs-12-en-28-oic acid
-
2,3-dibromo-1-(4-(hydroxy(oxido)amino)phenyl)-3-(4-quinolinyl)-1-propanone
-
2,4,6-trinitrophenyl-ATP
-
-
2,4,6-trinitrophenyl-CTP
-
-
2,4,6-trinitrophenyl-GTP
-
-
2,4,6-trinitrophenyl-UTP
-
-
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-(furanyl)-7,8-dihydro-5(6H)-quinazolinone
-
-
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
2OH-17beta estradiol
-
inhibits bicarbonate-induced cAMP production
3'-dATP
-
competitive inhibition
3'-deoxy-2'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
-
-
3'-deoxy-2'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
-
-
3'-methylanthraniloyl-2'-d-ATP
-
-
3'-O-(5-acetamidoanthraniloyl)-ATP
-
-
3'-O-(5-acetamidoanthraniloyl)-ITP
-
-
3'-O-(5-bromoanthraniloyl)-ADP
-
-
3'-O-(5-bromoanthraniloyl)-ATP
-
-
3'-O-(5-bromoanthraniloyl)-ITP
-
-
3'-O-(5-chloroanthraniloyl)-ATP
-
-
3'-O-(5-chloroanthraniloyl)-ITP
-
-
3'-O-(5-propylanthraniloyl)-ATP
-
-
3'-O-(5-propylanthraniloyl)-ITP
-
-
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
3-[(9-oxo-9H-fluorene-1-carbonyl)-amino]-benzoic acid
-
-
4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid
-
-
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'-benzyl-12'-hydroxy-2'-methyl-3',6',18-trioxoergotaman
-
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
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
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-arabinofuranosyladenine
-
-
9-CPA
-
a adenylate cyclase P-site inhibitor
9-tetrahydro-2'-furyladenine
-
effective and specific inhibitor for ACA in cell lysates and intact cells
9-[2-(phosphonomethoxy)ethyl]adenine diphosphate
-
-
alpha,beta-methylene adenosine 5'-triphosphate
-
in presence of diphosphate
alpha-cyano-(3,4,5-trihydroxy)cinnamonitrile
-
effective and specific inhibitor for ACG in cell lysates
beta, gamma subunit of the guanine-nucleotide binding regulatory protein
-
bis-acetamido-anthraniloyl-ITP
-
-
bithionol
potent, isoform Adcy10-specific inhibitor, noncompetitive with respect to ATP
buprenorphine
-
a low-efficacy partial mu-opioid agonist
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
calmodulin-dependent protein kinase II
-
in vivo
-
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
Co2+
-
high concentrations
cyclic poly-phosphate 17
-
-
cytidine 5'-(gamma-thio)triphosphate
-
-
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
-
di-methylanthraniloyl-IMP
-
-
epinephrine
-
overexposure to epinephrine inactivates adenylate cyclase
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
-
Gialpha
-
inhibits AC5 and AC6
-
guanosine 5'-(beta,gamma-imido)triphosphate
guanosine 5'-(gamma-thio)triphosphate
-
-
Hexachlorophene
potent, isoform Adcy10-specific inhibitor, noncompetitive with respect to ATP
HgCl2
-
inhibitory at 100microM
inosine 5'-(beta,gamma-imido)triphosphate
-
-
inosine 5'-(gamma-thio)triphosphate
-
-
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
methylanthraniloyl-ADP
-
-
methylanthraniloyl-ATP
-
-
methylanthraniloyl-ATPgammaS
-
-
methylanthraniloyl-CDP
-
-
methylanthraniloyl-CTP
-
-
methylanthraniloyl-GDP
-
-
methylanthraniloyl-GTP
-
-
methylanthraniloyl-GTPgammaS
-
-
methylanthraniloyl-IDP
-
-
methylanthraniloyl-IMP
-
-
methylanthraniloyl-ITP
-
-
methylanthraniloyl-ITPgammaS
-
-
methylanthraniloyl-UDP
-
-
methylanthraniloyl-UTP
-
-
morphine
-
a higher efficacy mu-opioid agonist
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
NaHCO3
-
approximately 50% inhibition of enzyme activity by 50 mM NaHCO3
nalbuphine
-
a low-efficacy partial mu-opioid agonist
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
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
-
oxaloacetate
Nocardia erythropolis
-
-
PAPANANOATE
-
nitric oxide donor, completely abolishes A2bR mediated cAMP production
pertussis toxin
chronic treatment of HEK-293T cells reduces AC5 activity
-
PKC
-
inhibits AC6 activity
-
Ribonucleoside triphosphates
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
thrombin
-
thrombin transiently inhibits adenylyl cyclase 6
-
U50488H
-
kappa opioid receptor agonist
U69593
-
kappa opioid receptor agonist
uridine 5'-(beta,gamma-imido)triphosphate
-
-
uridine 5'-(gamma-thio)triphosphate
-
-
vitamin D
-
decreases parathyroid-induced stimulation of AC6 and induces a phosphorylation of AC6 in a PKC-dependent manner
xanthosine 5'-(beta,gamma-imido)triphosphate
-
-
xanthosine 5'-(gamma-thio)triphosphate
-
-
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)-ATP
-
catalytic heterodimer VC1-IIC2
2'(3')-O-(N-methylanthraniloyl)-ATP
competitive
2'(3')-O-(N-methylanthraniloyl)-ATP
-
-
2'(3')-O-(N-methylanthraniloyl)-ATP
-
catalytic heterodimer VC1-IIC2
2'(3')-O-(N-methylanthraniloyl)-GTP
-
catalytic heterodimer VC1-IIC2
2'(3')-O-(N-methylanthraniloyl)-GTP
-
-
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
-
-
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'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
-
-
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
-
2',3'-O-(2,4,6-trinitrophenyl)-ADP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
-
2',3'-O-(2,4,6-trinitrophenyl)-AMP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
most potent inhibitor for isoform ACV
2',3'-O-(2,4,6-trinitrophenyl)-ATP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-CTP
-
-
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)-GDP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
-
2',3'-O-(2,4,6-trinitrophenyl)-GDP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
-
2',3'-O-(2,4,6-trinitrophenyl)-GTP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
catalytic heterodimer VC1-IIC2
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
most potent inhibitor for isoforms ACI and ACII
2',3'-O-(2,4,6-trinitrophenyl)-UTP
-
catalytic heterodimer VC1-IIC2
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
-
mixed-type inhibition
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'-deoxyadenosine
-
-
2-hydroxyestradiol
-
IC50 of about 2 microM
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
significant inhibition at 0.1 mM
2-hydroxyestradiol
-
0.01 mM used in assay conditions
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
-
-
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
3'-AMP
Nocardia erythropolis
-
-
4-hydroxyestradiol
-
-
4-hydroxyestradiol
-
reversible inhibition of recombinant soluble enzyme in dose dependent manner, IC50 in low micromolar range
4-hydroxyestradiol
-
a catechol estrogen and sAC-selective inhibitor
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
adenosine
-
-
ATP
-
high concentrations
ATP
-
high concentrations
ATP
-
high concentrations
ATP
-
substrate inhibition at high concentrations, inhibition is relieved in the presence of HCO3-, no substrate inhibition in the presence of 50 mM HCO3-
ATP
-
high concentrations
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
BAPTA
-
inhibits calcium-stimulated AC
beta, gamma subunit of the guanine-nucleotide binding regulatory protein
-
-
-
beta, gamma subunit of the guanine-nucleotide binding regulatory protein
-
-
-
Ca2+
-
-
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+
-
isoforms AC5 and AC6 are inhibited by Ca2+
Ca2+
-
type V adenylyl cyclase
Ca2+
-
addition of Ca2+ to cells which have been depleted of intracellular Ca2+ markedly suppress cAMP synthesis by AC9
Ca2+
calcium-inhibited AC5 isozyme
Ca2+
-
Ca2+ stimulates transmembrane isozymes AC1 and AC8 via calmodulin, and inhibits AC5 and AC6 directly
Ca2+
-
inhibits isoforms AC5 and AC6, but not isoform AC4
Ca2+
-
inhibits isoform AC6
Ca2+
-
cortical adenylyl cyclase AC5 is sensitive to inhibition by Ca2+
Ca2+
-
type II adenylyl cyclase
Ca2+
-
bradykinin receptor-mediated increases in the release of intracellular calcium inhibits AC6 activity
Ca2+
-
capacitative operated Ca2+ entry inhibits AC6
Ca2+
-
calcium entrance in the cell inhibits the enzyme
Ca2+
-
at 0.1 mM and higher, the calcium cations inhibit the adenylyl cyclase activity
cAMP
-
mutant K372A shows at least 20fold increase in the IC50 value
cAMP
-
in presence of diphosphate
catechol
-
noncompetetive inhibitor
catechol
-
and derivatives
Chloropromazine
-
-
CTP
-
-
CTP
Nocardia erythropolis
-
-
DAMGO
-
a higher efficacy mu-opioid agonist
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
diphosphate
-
no difference between wild type and mutant K372A
diphosphate
-
non-competitive inhibitor with respect to ATP
EGTA
-
-
EGTA
-
freshly activated CyaA is inhibited by EGTA at low calmodulin concentrations
F-
-
-
GTP
-
-
GTP
Nocardia erythropolis
-
-
GTP
competitive inhibition
guanosine 5'-(beta,gamma-imido)triphosphate
-
at low concentrations
guanosine 5'-(beta,gamma-imido)triphosphate
-
-
inhibitory G protein
-
-
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
-
inhibitory G protein
-
-
-
ITP
-
-
ITP
Nocardia erythropolis
-
-
KH2PO4
-
-
KH7
-
potent, specific inhibitor
KH7
-
sAC-specific inhibitor
MANT-GTP
-
inhibits the VC1-IIC2 heterodimer
MANT-GTP
-
inhibits the VC1-IIC2 heterodimer
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
MDL 12330A
-
specific transmembrane adenylyl cyclase inhibitor
Mercuric acetate
-
-
Mg2+
-
-
Mg2+
-
high concentrations
Mn2+
Nocardia erythropolis
-
-
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
catalytic heterodimer VC1-IIC2
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
-
catalytic heterodimer VC1-IIC2
NaCl
-
-
NaCl
reduced enzyme activity in the presence of 500 mM NaCl
NADH
-
-
NaF
-
-
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
nucleotides
-
-
-
pyridoxal 5'-phosphate
-
-
pyridoxal 5'-phosphate
-
-
pyridoxal 5'-phosphate
Nocardia erythropolis
-
-
quinpirole
-
-
quinpirole
-
inhibits the enzyme via Gi protein
Ribonucleoside triphosphates
-
-
Ribonucleoside triphosphates
-
-
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
-
decreases cAMP production despite the presence of UTP
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
SQ22536
-
a adenylate cyclase P-site inhibitor
SQ22536
-
selective non-competitive inhibitor of adenylyl cyclase
Trifluoperazine
-
-
tyrphostin A25
-
IC50 0.119mM, IC50 forskolin-stimulated adenylyl cyclase 1 mM, 37°C, pH 7.5
tyrphostin A25
IC50 of about 36 microM
UTP
-
-
UTP
Nocardia erythropolis
-
-
Zn2+
-
-
Zn2+
0.007 mM, 50% inhibition
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
-
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
-
not inhibitory: estrone and estrogen
-
additional information
-
not inhibited by 17beta-estradiol
-
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
-
structure-activity relationship
-
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
-
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
-
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
-
additional information
-
NaCl, KCl not inhibitory
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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
1,6-anhydro-MurNAc-L-Ala-D-Glu
-
-
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
5'-guanylimidodiphosphate
5,5'-dimethyl-1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetra-acetic acid
5-CT
-
h5-HT6/rAC2 cell line highly responsive
5-HT
-
h5-HT6/rAC2 cell line highly responsive
5-hydroxytryptamine
-
stimulation of enzyme activity up to 2.5fold
A-77636
-
a dopamine receptor agonist, the activation by can be reversed by D1-receptor antagonists SCH23390, SKF83566, and butaclamol
A23187
-
activates isozymes AC-I and AC-III
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
adrenaline
-
stimulates adenylate cyclase activity
alpha subunit of the guanine-nucleotide binding regulatory protein
-
arachidonic acid
strong activation at 0.1 mM
bacterial peptidoglycan
-
direct activation of Cyr1p
-
BIM-1
-
specific protein-kinase C inhibitor, significantly increases cumulus cell cAMP concentrations
bovine serum albumin
-
stimulation
-
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
clonidine
-
slight stimulatory effect on cAMP concentrations
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
D1A dopamine receptor
-
-
-
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+
-
EGTA
-
significantly increases cumulus cell cAMP concentrations
G protein subunit
-
requirement for dual regulation of the AC by both Gs activation and Ca2+/calmodulin in a time-dependent manner
-
G-protein alpha-subunit
-
-
-
G-protein coupled receptor
-
-
-
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'-(beta,gamma-imido)triphosphate
guanosine 5'-(gamma-thio)triphosphate
-
stimulation of enzyme activity up to 3.5fold
guanosine diphosphate methylene phosphate
-
activation
H89
-
specific inhibitor of protein-kinase A, significantly increases cumulus cell cAMP concentrations at 0.0001 and 0.03 mM
IBMX
-
increases basal renin release
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
light
-
the enzyme is light-activated
-
linoleic acid
strong activation at 0.1 mM
linolenic acid
strong activation at 0.1 mM
lisuride
-
h5-HT6/rAC2 cell line highly responsive
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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1647 is slightly activated at 500 mM
NaHCO3
-
10 mM, 30fold activation, half-maximal activation at 11 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
NKH 477
-
application of NKH 477, a water-soluble forskolin analog, stimulates membrane-bound adenylyl cyclase
oleic acid
strong activation at 0.1 mM
palmitic acid
stimulates 3fold
phorbol 12-myristate 13-acetate
-
PKC-selective activator, stimulates AC2
pituitary adenylate cyclase activating polypeptide
-
-
-
pituitary adenylate cyclase-activating polypeptide
-
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
-
relaxin
-
AC5 activity is potentiated by PKCzeta after exposure to relaxin
-
sphingosine 1-phosphate
stimulates
staurosporine
-
non-specific protein-kinase C inhibitor, significantly increases cumulus cell cAMP concentrations
sumatriptan
-
h5-HT6/rAC2 cell line highly responsive
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
-
Vasoactive intestinal peptide
[8-arginine]vasopressin
-
0.01 mM [8-arginine]vasopressin significantly activates cortical and medulla adenylyl cyclase
-
5'-guanylimidodiphosphate
-
activation
5'-guanylimidodiphosphate
-
activation
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
-
A2bR
-
cAMP production induced only in cells transfected with A2bR
-
alpha subunit of the guanine-nucleotide binding regulatory protein
-
activation
-
alpha subunit of the guanine-nucleotide binding regulatory protein
-
activation
-
alpha subunit of the guanine-nucleotide binding regulatory protein
-
activation
-
bicarbonate
-
1.36fold stimualtion of activity at 40 mM
bicarbonate
-
stimulates 2.5fold
bicarbonate
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 stimulates purified Rv1319c catalytic domain
bicarbonate
activates CyaB1 2.5fold
bicarbonate
-
1.63fold stimualtion of activity at 40 mM
bicarbonate
-
activates sAC in vivo and in vitro in a pH-dependent manner
bicarbonate
-
50 mM stimulate sAC activity 2fold
Calmodulin
-
requirement for dual regulation of the AC by both Gs activation and Ca2+/calmodulin in a time-dependent manner
Calmodulin
-
required for activity
Calmodulin
-
strong activation
Calmodulin
-
maximal activity at 0.001 mM
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
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
Drosophila sp. (in: flies)
-
-
Calmodulin
-
stimulates AC8
Calmodulin
-
stimulates the soluble isozyme
Calmodulin
-
Ca2+/calmodulin enhance cAMP production through AC9
Calmodulin
-
stimulates AC1 and AC8 in a Ca2+-dependent manner
Calmodulin
AC1 activity is regulated by both Ca2+/calmodulin and G proteins
Calmodulin
activates isozyme AC1
Calmodulin
activates isozyme AC8
Calmodulin
Ca2+/calmodulin-stimulated isozyme AC1
Calmodulin
Ca2+/calmodulin-stimulated isozyme AC8
Calmodulin
isozyme AC8 is a pure Ca2+/calmodulin sensor
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
-
no detectable stimulation of enzyme activity
Calmodulin
-
stimulates AC8 in a Ca2+-dependent manner
Calmodulin
Ca2+ stimulates transmembrane isozyme AC8 via calmodulin
cAMP
activation of recombinant cyaB1 via N-terminal GAF domains
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+
catecholamine
-
activation
catecholamine
-
activation
CO2
-
-
CO2
-
synergistic effects of synthetic muramyl dipeptides and CO2
CO2
-
induces acidification of cells, accompanied by a rise in intracellular HCO3-
CO2
-
stimulates 2fold at 20 mM at pH 7.5
dopamine
-
about 2fold activation by 0.1 mM
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
-
increases cAMP accumulation in a GTP-dependent manner, enhances AC5 activity via phosphorylation of Galphas on one or more tyrosine residues
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
epinephrine
-
about 2fold activation by 0.1 mM
epinephrine
-
significantly activates cortical adenylyl cyclase
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
-
potentiates AC7 activity through a PKC-delta-mediated phosphorylation
ethanol
-
stimulates isoform AC6, AC7 and AC9 activity
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
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
forskolin
-
slight activation, recombinant CyaB1-maltose binding protein fusion
forskolin
-
increases substantially cAMP concentrations
forskolin
-
catalytic heterodimer VC1-IIC2
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
-
decreased forskolin-stimulated adenylyl cyclase activity in suicide subjects
forskolin
-
forskolin-sensitive isozymes
forskolin
-
free G protein Gsalpha subunits enhance adenylate cyclase responses to forskolin
forskolin
-
leads to cAMP accumulation in C6 glioma cells expressing the mu-opioid-receptor
forskolin
-
structure-activity relationship
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
-
binds to the cytoplasmic domains, structure overview. Isozyme group IV contains forskolin-insensitive isozyme AC9, mode of regulation, overview
forskolin
-
strong activation
forskolin
-
stimulates an 11fold increase in cAMP
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
-
increases the number of active synapses
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
-
scarcely enhanced enzyme activity
forskolin
-
significantly activates cortical adenylyl cyclase
forskolin
-
catalytic heterodimer VC1-IIC2
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
-
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
activates the transmembrane isozyme
forskolin
-
activation in a Mg2+-dependent manner
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
-
direct adenylate cyclase agonist, causes smaller increases in contraction and Ca2+ transient amplitudes in aged compared to younger ventricular myocytes
forskolin
-
forskolin activation is elevated by nicotine treatment in adolescence, especially in males
forskolin
-
increases the number of active synapses
forskolin
-
scarcely stimulated enzyme activity
forskolin
-
stimulates tmAC activity 1.6fold
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
activation by betagamma subunits
-
G-protein
betagamma subunit
-
G-protein
betagamma subunits
-
Galphas
-
-
Galphas
-
catalytic heterodimer VC1-IIC2
-
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 the VC1-IIC2 heterodimer
-
Galphas
-
stimulates Gbetagamma subunits whereby enhancing the activity of enzymes
-
Galphas
-
catalytic heterodimer VC1-IIC2
-
Galphas
-
stimulates the VC1-IIC2 heterodimer
-
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
-
Gbetagamma
-
stimulates AC2
-
Gbetagamma
-
conditionally stimulates ACV and ACVI
-
glucagon
-
activation
glucagon
-
0.04 mM glucagon significantly activates cortical and medulla adenylyl cyclase
Gsalpha
signal transduction from beta-adrenergic receptors via trimeric Gs proteins to their downstream targets, e.g. ACs
-
Gsalpha
-
AC5 undergoes a cooperative activation by Gsalpha
-
GTP
-
activation
GTP-gamma-S
-
activation
GTPgammaS
-
-
GTPgammaS
-
a nonhydrolysable GTP analogue, increases AC activity
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
GTPgammaS
-
stimulation of activity occurs at 0.005 mM
GTPgammaS
-
up to 14fold stimulation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
guanosine 5'-(beta,gamma-imido)triphosphate
-
activation
HCO3-
-
-
HCO3-
-
mediates cAMP production
HCO3-
-
the enzyme is directly activated by bicarbonate
HCO3-
-
50 mM, 5-20fold activation in the presence of Mg2+, 3fold activation in the presence of Mn2+
HCO3-
-
sAC stimulation increases more than 2fold between pH 7 and 8
HCO3-
-
50 mM, 5-20fold activation in the presence of Mg2+, 3fold activation in the presence of Mn2+
isoprenaline
-
-
isoproterenol
-
-
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
-
significantly activates cortical adenylyl cyclase
isoproterenol
-
stimulates AC6 resulting in a significant increase in the arborization process
NaF
-
activation
NaF
-
activates the transmembrane isozyme, but not the soluble isozyme
NaF
-
stimulates tmAC activity 2.9fold
NKH477
-
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
NKH477
-
a water soluble forskolin analogue that directly stimulates AC
norepinephrine
-
norepinephrine
activates endogenously expressed b-adrenergic receptors, signal transduction from beta-adrenergic receptors via trimeric Gs proteins to their downstream targets, e.g. ACs
norepinephrine
-
about 2fold activation by 0.1 mM
norepinephrine
-
significantly activates cortical adenylyl cyclase
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
-
-
-
pituitary adenylate cyclase-activating polypeptide
-
-
-
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
-
PMA
-
potentiates drug-stimulated cAMP accumulation
PMA
-
potentiates drug-stimulated cAMP accumulation
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
-
significant stimulation of enzyme activity
serotonin
-
the stimulatory effect of serotonin on adenylyl cyclase activity (253%) is enhanced in the presence of 0.005 mM Ca2+
SKF-82958
-
-
SKF-82958
-
a D1 dopaminergic receptor agonist
Sodium fluoride
-
-
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
-
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
-
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
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
-
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
-
-
-
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
Vasoactive intestinal peptide
-
activation
Vasoactive intestinal peptide
-
activation
Vasopressin
-
-
Vasopressin
-
causes halfmaximal stimulation of cAMP accumulation
additional information
-
not activated by forsoklin
-
additional information
-
not activated by cAMP
-
additional information
-
not activated by HCO3-
-
additional information
neither ionomycin nor thapsigargin activate
-
additional information
-
neither ionomycin nor thapsigargin activate
-
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
-
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
-
blue-light irradiation activates the AC 80fold
-
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
-
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
-
phosphorylation of a C-terminally located threonine residue increases activity of AC2 in intact HEK-293 cells
-
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
-
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
-
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
-
isoenzyme AC9 is not activated by forskolin
-
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
-
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
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
-
superactivation method for the isozymes, overview
-
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
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
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
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
-
Rv1264 is a pH-regulated enzyme
-
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
-
the transmembrane isozyme is induced by light, overview
-
additional information
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
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
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
-
not activated by histamine and 5-HT
-
additional information
-
not activated by forsoklin
-
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
-
chronic treatment with mu-opioid agonists leads to upregulation of the of the cAMP-signalling pathway
-
additional information
-
measurement of dopamine receptor agonist activation in a competitive assay with antagonists, e.g. SCH23390, overview
-
additional information
netrin-1 does not alter cAMP levels in axons attracted by this cue
-
additional information
-
no activation of the soluble isozyme by the transmembrane isozyme-specific activator forskolin
-
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
-
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
-
additional information
-
not activated by HCO3-
-
additional information
-
Ras-GTP and mediates activation of the AC
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
0.33
adenylimidodiphosphate
-
-
1.38
GTP
Q7CH76
wild type enzyme, pH 8.5, 37°C
additional information
additional information
-
0.0005
ATP
-
-
0.001
ATP
transmebrane isozyme
0.0022
ATP
-
native Cya1, pH 7.5, 27°C
0.0022
ATP
-
pH 7.5, 27°C
0.0027
ATP
-
truncated Cya1, pH 7.5, 27°C
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
0.0067
ATP
-
recombinant CyaB1-maltose binding protein fusion
0.011
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 2 mM Mn2+
0.011
ATP
-
wild type isoform V, 30°C
0.011
ATP
Q7CH76
mutant enzyme R63A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.0114
ATP
-
in the presence of Cl-
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
0.0162
ATP
-
in the presence of HCO3-
0.02
ATP
Q7CH76
wild type enzyme, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.021
ATP
-
wild type isoform VI, 30°C
0.024
ATP
37°C, pH 7.5, recombinant cyaB1 AC, in the presence of 10 mM Mg2+ and 0.1 mM cAMP
0.026
ATP
-
mutant isoform V N1090D, 30°C
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
0.0327
ATP
-
truncated Cya1, pH 7.5, 27°C, 50 mM NaHCO3
0.0339
ATP
-
native Cya1, pH 7.5, 27°C, 50 mM NaHCO3
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+
0.039 - 0.051
ATP
-
normal and rous sarcoma transformed
0.045
ATP
-
in the presence of Mn2+
0.046
ATP
Q7CH76
mutant enzyme K76A, in the presence of 10 mM Mn2+, at pH 8.5 and 37°C
0.048
ATP
-
mutant isoform VI F1078S, 30°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
0.0667
ATP
-
pH 8.5, 40°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
-
membrane-bound ACs
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
0.14
ATP
-
wild type, pH 8.0, 25°C
0.15
ATP
-
S49 cyc-, pH 7.4, 37°C, Mn2+, 100 microM forskolin
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+
0.17
ATP
-
mutant H351N, pH 8.0, 25°C
0.19
ATP
-
mutant H351F, pH 8.0, 25°C
0.2
ATP
Nocardia erythropolis
-
-
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
0.21
ATP
Q7CH76
wild type enzyme, at pH 7.0, in Tris buffer at 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+
0.27
ATP
pH 8.0, 37°C, recombinant catalytic domain, 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+
0.3
ATP
-
30°C, pH 7.2, 2 microM free Ca2+
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+
0.34
ATP
Q7CH76
wild type enzyme, at pH 8.0, in Tris buffer at 37°C
0.37
ATP
Q7CH76
wild type enzyme, at pH 7.5, in Tris buffer at 37°C
0.398
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant T189A, 10 mM Mg2+
0.4
ATP
recombinant TczAC
0.4
ATP
-
mutant VC1-A406P+IIC2-I1006V, 30°C, pH 7.4, 10 mM MnCl, 0.1 mM forskolin
0.4
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mn2+
0.4
ATP
Q7CH76
mutant enzyme K76A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.427
ATP
-
25°C, plasma membrane isolated from lactic acid grown cells
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
0.43
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM MnCl, 0.1 mM forskolin
0.43
ATP
Q7CH76
wild type enzyme, at pH 8.5, in Tris buffer at 37°C
0.44
ATP
Q7CH76
wild type enzyme, at pH 9.0, in Tris buffer at 37°C
0.46
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant R19A, 10 mM Mg2+
0.53
ATP
-
mutant VC1-A409P+IIC2, 30°C, pH 7.4, 10 mM MnCl, 0.1 mM forskolin
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+
0.56
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mg2+, 0.1 mM forskolin
0.57
ATP
-
mutant VC1+IIC2-I1006V, 30°C, pH 7.4, 10 mM MnCl, 0.1 mM forskolin
0.6
ATP
-
recombinant C-terminal cytoplasmic domain of type II adenylyl cyclase
0.6
ATP
-
recombinant cytosolic domain of type V adenylyl cyclase
0.6
ATP
-
wild type enzyme, at pH 8.0 and 30°C
0.609
ATP
-
in the presence of Mg2+
0.62
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mn2+, 0.1 mM forskolin
0.62
ATP
Q7CH76
mutant enzyme C83A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
0.68
ATP
-
recombinant form VC1-IIC2, 30°C, pH 7.4, 10 mM Mg2+
0.682
ATP
pH 8.0, 37°C, recombinant catalytic domain mutant K332A, 10 mM Mg2+
0.69
ATP
Q7CH76
wild type enzyme, at pH 9.5, in Tris buffer at 37°C
0.7
ATP
Q7CH76
wild type enzyme, at pH 10.0, in Tris buffer at 37°C
0.71
ATP
Q7CH76
wild type enzyme, at pH 10.4, in Tris buffer at 37°C
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
0.82
ATP
-
pH 7.4, 22°C, 5mM Mg2+
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
0.97
ATP
recombinant cyaC
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
1.2
ATP
sAC activity in cytosolic extracts in the presence of Mn2+
1.3
ATP
-
30°C, pH 7.2, 0.1 microM free Ca2+
1.5
ATP
-
mutant enzyme R338A/D360A, at pH 8.0 and 30°C
1.89
ATP
Q7CH76
mutant enzyme F5A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
2.2
ATP
-
mutant enzyme N347A, at pH 8.0 and 30°C
2.29
ATP
Q7CH76
mutant enzyme L72A, in the presence of 20 mM Mg2+, at pH 8.5 and 37°C
2.4
ATP
-
high molecular weight form
3
ATP
-
mutant enzyme R338A/D360A, at pH 8.0 and 30°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+
5
ATP
-
recombinant protein
0.009
MgATP2-
-
in presence of almathicin
0.019
MgATP2-
-
in absence of amathicin
0.067
MnATP2-
-
-
additional information
additional information
-
-
-
additional information
additional information
-
-
-
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
-
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0.000011 - 0.05
2'(3')-O-(N-methylanthraniloyl)-ATP
0.00006 - 0.000872
2'(3')-O-(N-methylanthraniloyl)-ATPgammaS
0.000051 - 0.004141
2'(3')-O-(N-methylanthraniloyl)-CTP
0.000013 - 0.001249
2'(3')-O-(N-methylanthraniloyl)-GTP
0.000027 - 0.000666
2'(3')-O-(N-methylanthraniloyl)-GTPgammaS
0.000006 - 0.00003
2'(3')-O-(N-methylanthraniloyl)-ITP
0.00001 - 0.00005
2'(3')-O-(N-methylanthraniloyl)-ITPgammaS
0.000022 - 0.0015
2'(3')-O-(N-methylanthraniloyl)-UTP
0.0055
2',3'-bis[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
0.0067
2',3'-di[(2-(N-methylanthraniloyl)amino)ethyl-carbamoyl]-ATP
0.00014 - 0.002
2',3'-O-(2,4,6-trinitrophenyl)-ADP
0.0048 - 0.021
2',3'-O-(2,4,6-trinitrophenyl)-AMP
0.0000037 - 0.0001
2',3'-O-(2,4,6-trinitrophenyl)-ATP
0.000024 - 0.00031
2',3'-O-(2,4,6-trinitrophenyl)-CTP
0.00041 - 0.0094
2',3'-O-(2,4,6-trinitrophenyl)-GDP
0.000023 - 0.00043
2',3'-O-(2,4,6-trinitrophenyl)-GTP
0.0000071 - 0.000092
2',3'-O-(2,4,6-trinitrophenyl)-UTP
0.00064 - 0.0029
2',3'-O-(N-anthraniloyl)-ADP
0.00012 - 0.00064
2',3'-O-(N-anthraniloyl)-ATP
0.0043 - 0.0075
2',3'-O-(N-anthraniloyl)-IMP
0.00079 - 0.0029
2',3'-O-(N-methylanthraniloyl)-ADP
0.0001 - 0.00033
2',3'-O-(N-methylanthraniloyl)-ATP
0.00058 - 0.0037
2',3'-O-(N-methylanthraniloyl)-CDP
0.00015 - 0.00069
2',3'-O-(N-methylanthraniloyl)-CTP
0.000053 - 0.00061
2',3'-O-(N-methylanthraniloyl)-GTP
0.000034 - 0.00037
2',3'-O-(N-methylanthraniloyl)-GTPgammaS
0.000031 - 0.000086
2',3'-O-(N-methylanthraniloyl)-IDP
0.0044 - 0.0085
2',3'-O-(N-methylanthraniloyl)-IMP
0.0000012 - 0.000014
2',3'-O-(N-methylanthraniloyl)-ITP
0.000032 - 0.00012
2',3'-O-(N-methylanthraniloyl)-ITPgammaS
0.00034 - 0.0027
2',3'-O-(N-methylanthraniloyl)-UDP
0.000032 - 0.00046
2',3'-O-(N-methylanthraniloyl)-UTP
0.0011 - 0.003
2',3'-O-(N-methylanthraniloyl)-XTP
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
0.00032 - 0.0048
2'-deoxy-3'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
0.00027 - 0.0013
2'-deoxy-3'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
0.0003 - 0.022
2'-methylanthraniloyl-3'-d-ATP
0.0065 - 0.11
2,4,6-trinitrophenyl-ATP
0.01 - 0.41
2,4,6-trinitrophenyl-CTP
0.02 - 0.32
2,4,6-trinitrophenyl-GTP
0.058 - 0.78
2,4,6-trinitrophenyl-UTP
0.000065 - 0.00054
3'-deoxy-2'-O-[2-(methylamino)benzoyl]adenosine 5'-triphosphate
0.0018 - 0.0087
3'-deoxy-2'-O-[2-(methylamino)benzoyl]guanosine 5'-triphosphate
0.0002 - 0.032
3'-methylanthraniloyl-2'-d-ATP
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
0.0094 - 0.01
8-[(4-(N-methylanthraniloyl)amino)butyl]amino-ATP
0.058 - 0.1
8-[(6-(N-methylanthraniloyl)amino)hexyl]-amino-ATP
0.000001 - 0.000025
9-[2-(phosphonomethoxy)ethyl]adenine diphosphate
0.011 - 0.1
anthraniloyl-ADP
0.0013 - 0.02
anthraniloyl-ATP
0.029 - 0.1
anthraniloyl-GTP
0.0075
bis-acetamido-anthraniloyl-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.033 - 0.071
cytidine 5'-(gamma-thio)triphosphate
0.02 - 0.037
di-methylanthraniloyl-IMP
2.4 - 3
guanosine 5'-(beta,gamma-imido)triphosphate
0.4 - 0.41
guanosine 5'-(gamma-thio)triphosphate
0.35 - 0.48
inosine 5'-(beta,gamma-imido)triphosphate
0.02 - 0.021
inosine 5'-(gamma-thio)triphosphate
0.077
ITPgammaS
-
in the presence of Mn2+
0.012 - 0.091
methylanthraniloyl-ADP
0.0043 - 0.051
methylanthraniloyl-ATP
0.0012 - 0.015
methylanthraniloyl-ATPgammaS
0.018 - 0.1
methylanthraniloyl-CDP
0.0011 - 0.036
methylanthraniloyl-CTP
0.06
methylanthraniloyl-GDP
-
in the presence of Mn2+
0.0059 - 0.016
methylanthraniloyl-GTP
0.0054 - 0.0074
methylanthraniloyl-GTPgammaS
0.011 - 0.1
methylanthraniloyl-IDP
0.1
methylanthraniloyl-IMP
0.0006 - 0.016
methylanthraniloyl-ITP
0.0018 - 0.031
methylanthraniloyl-ITPgammaS
0.043 - 0.1
methylanthraniloyl-UDP
0.0026 - 0.042
methylanthraniloyl-UTP
0.0094 - 0.011
N6-[6-((N-methylanthraniloyl)amino)hexyl]-ATP
2.5 - 2.8
uridine 5'-(beta,gamma-imido)triphosphate
0.015 - 0.051
uridine 5'-(gamma-thio)triphosphate
0.036
UTPgammaS
-
in the presence of Mn2+
10
xanthosine 5'-(beta,gamma-imido)triphosphate
0.02 - 0.025
xanthosine 5'-(gamma-thio)triphosphate
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
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 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
0.0003
2'-methylanthraniloyl-3'-d-ATP
-
in the presence of Mn2+
0.022
2'-methylanthraniloyl-3'-d-ATP
-
in the presence of Mg2+
0.0065
2,4,6-trinitrophenyl-ATP
-
in the presence of Mn2+
0.11
2,4,6-trinitrophenyl-ATP
-
in the presence of Mg2+
0.01
2,4,6-trinitrophenyl-CTP
-
in the presence of Mn2+
0.41
2,4,6-trinitrophenyl-CTP
-
in the presence of Mg2+
0.02
2,4,6-trinitrophenyl-GTP
-
in the presence of Mn2+
0.32
2,4,6-trinitrophenyl-GTP
-
in the presence of Mg2+
0.058
2,4,6-trinitrophenyl-UTP
-
in the presence of Mn2+
0.78
2,4,6-trinitrophenyl-UTP
-
in the presence of Mg2+
0.104
3'-dATP
-
wild type
0.132
3'-dATP
-
mutant H351N
0.146
3'-dATP
-
mutant H351F
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
0.0002
3'-methylanthraniloyl-2'-d-ATP
-
in the presence of Mn2+
0.032
3'-methylanthraniloyl-2'-d-ATP
-
in the presence of Mg2+
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+
0.011
anthraniloyl-ADP
-
in the presence of Mn2+
0.1
anthraniloyl-ADP
-
in the presence of Mg2+
0.0013
anthraniloyl-ATP
-
in the presence of Mn2+
0.02
anthraniloyl-ATP
-
in the presence of Mg2+
0.029
anthraniloyl-GTP
-
in the presence of Mn2+
0.1
anthraniloyl-GTP
-
in the presence of Mg2+
1.3
cAMP
-
forward reaction, 2 microM free Ca2+, pH 7.2, 30°C
1.5
cAMP
-
reverse reaction, 0.1 microM free Ca2+, pH 7.2, 30°C
2
cAMP
-
reverse reaction, 2 microM free Ca2+, pH 7.2, 30°C
3.7
cAMP
-
forward reaction, 0.1 microM free Ca2+, pH 7.2, 30°C
0.035
CTP
-
in the presence of Mn2+
0.27
CTP
-
in the presence of Mg2+
1
CTP
-
S49 cyc-, Mn2+, 100 microM forskolin
2.9
CTP
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
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
0.02
di-methylanthraniloyl-IMP
-
in the presence of Mn2+
0.037
di-methylanthraniloyl-IMP
-
in the presence of Mg2+
0.06
diphosphate
-
forward reaction, 2 microM free Ca2+, pH 7.2, 30°C
0.3
diphosphate
-
forward reaction, 0.1 microM free Ca2+, pH 7.2, 30°C
1
diphosphate
-
reverse reaction, 0.1 microM free Ca2+, pH 7.2, 30°C
1.2
diphosphate
-
reverse reaction, 2 microM free Ca2+, pH 7.2, 30°C
0.027
GTP
-
in the presence of Mn2+
0.26
GTP
-
in the presence of Mg2+
0.44
GTP
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
0.67
GTP
-
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
0.1
ITP
-
in the presence of Mn2+
0.6
ITP
-
S49 cyc-, Mn2+, 100 microM forskolin
0.99
ITP
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
1.1
ITP
-
in the presence of Mg2+
0.012
methylanthraniloyl-ADP
-
in the presence of Mn2+
0.012
methylanthraniloyl-ADP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.091
methylanthraniloyl-ADP
-
in the presence of Mg2+
0.0043
methylanthraniloyl-ATP
-
in the presence of Mn2+
0.0043
methylanthraniloyl-ATP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.051
methylanthraniloyl-ATP
-
in the presence of Mg2+
0.0012
methylanthraniloyl-ATPgammaS
-
in the presence of Mn2+
0.015
methylanthraniloyl-ATPgammaS
-
in the presence of Mg2+
0.018
methylanthraniloyl-CDP
-
in the presence of Mn2+
0.1
methylanthraniloyl-CDP
-
in the presence of Mg2+
0.0011
methylanthraniloyl-CTP
-
in the presence of Mn2+
0.0011
methylanthraniloyl-CTP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.036
methylanthraniloyl-CTP
-
in the presence of Mg2+
0.0059
methylanthraniloyl-GTP
-
in the presence of Mn2+
0.016
methylanthraniloyl-GTP
-
in the presence of Mg2+
0.0054
methylanthraniloyl-GTPgammaS
-
in the presence of Mn2+
0.0074
methylanthraniloyl-GTPgammaS
-
in the presence of Mg2+
0.011
methylanthraniloyl-IDP
-
in the presence of Mn2+
0.011
methylanthraniloyl-IDP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.1
methylanthraniloyl-IDP
-
in the presence of Mg2+
0.1
methylanthraniloyl-IMP
-
in the presence of Mg2+
0.1
methylanthraniloyl-IMP
-
in the presence of Mn2+
0.0006
methylanthraniloyl-ITP
-
in the presence of Mn2+
0.0006
methylanthraniloyl-ITP
-
in 75 mM HEPES/NaOH, pH 7.4, at 25°C
0.016
methylanthraniloyl-ITP
-
in the presence of Mg2+
0.0018
methylanthraniloyl-ITPgammaS
-
in the presence of Mn2+
0.031
methylanthraniloyl-ITPgammaS
-
in the presence of Mg2+
0.043
methylanthraniloyl-UDP
-
in the presence of Mn2+
0.1
methylanthraniloyl-UDP
-
in the presence of Mg2+
0.0026
methylanthraniloyl-UTP
-
in the presence of Mn2+
0.042
methylanthraniloyl-UTP
-
in the presence of Mg2+
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
0.12
UTP
-
in the presence of Mn2+
0.33
UTP
-
in the presence of Mg2+
1.1
UTP
-
S49 cyc-, Mn2+, 100 microM forskolin
2.2
UTP
-
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
0.55
XTP
-
S49 cyc-, Mn2+, 100 microM forskolin
0.95
XTP
-
Sf9, Mn2+, 100 microM forskolin, 10 mM NaF, 10 microM AlCl3
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D650A
mutation in cyaB1-595-859 catalytical domain, no activity
L259V
affinity for cAMP is at least 11fold higher than for cGMP
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
N728A
mutation in cyaB1-595-859 catalytical domain, no activity
T258S
preference for cGMP over cAMP is 35fold, affinity for both cyclic nucleotides is enhanced
T258S/L259V
response to cGMP is highly diminished
K533E/I603R/D605C
mutant lose adenylyl cyclase activity but obtains significant guanylyl cyclase activity
H351A
-
mutant with no enzyme activity
H351F
-
mutant with 40fold decreased enzyme activity
H351N
-
mutant with 34fold decreased enzyme activity
K372A
-
mutant with 30fold reduced catalytic rate constant and 3fold increased Km value for ATP
A225C
a CyaA 1-373 mutant
N347A
-
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
-
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
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
D414B
-
mutant does not show increased cAMP levels
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
G463D
-
mutant does not show increased cAMP levels
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
R188H
-
mutant does not show increased cAMP levels
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
F1078S
-
isoform VI, mutation within the GALPHAS binding pocket
N1090D
-
isoform V, mutation within the GALPHAS binding pocket
N955A
-
mutation prevents glycosylation
N964A
-
mutation prevents glycosylation
Y1082L
-
mutation in AC9 confers both binding and activation by forskolin
D147A
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1647 mutant, mutation of first metal-binding residue, barely active
D241C
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
D256A
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 mixture of artificial C2-like mutants of Rv1625c, reconstitutes an active enzyme
D300A
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
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
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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
K187E/D241C
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1647 mutant, mixture of artificial C1-like mutants, reconstitutes high adenylyl cyclase activity, does not lead to a gain in guanylyl cyclase activity
K296A
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 mixture of artificial C1-like mutants of Rv1625c, reconstitutes an active enzyme
Q57K/N106D
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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+
R309A
mutation renders holoenzyme active and unregulated
R31G
118% of wild-type activity, in the presence of 2 mM Mn2+
R376A
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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+
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
-
Rv1647 mutant, mutation of first metal-binding residue, barely active
-
D241C
-
Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
-
D256A
-
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
-
D365A
-
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
-
Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
-
E136A
-
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
-
mutant with poor adenylate cyclase acitivity
-
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
-
K187E
-
Rv1647 mutant, mutation of C1-like substrate specifying residues, barely active, does not lead to a gain in guanylyl cyclase activity
-
K187E/D241C
-
Rv1647 mutant, mixture of artificial C1-like mutants, reconstitutes high adenylyl cyclase activity, does not lead to a gain in guanylyl cyclase activity
-
K296E/D365C
-
double mutant with severely compromised enzyme activity
-
K296E/F363R/D365C
-
triple mutant with severely compromised enzyme activity
-
Q57K/N106D
-
Rv0386 mutant, abolishes activity
-
R132A
-
shift of the pH optimum by about 0.5 unit to acidic pH
-
R18A
-
88% 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+
-
R309A
-
mutation renders holoenzyme active and unregulated
-
R43A/R44G
-
1.3% of wild-type activity, in the presence of 2 mM Mn2+
-
R4G
-
77% of wild-type activity, in the presence of 2 mM Mn2+
-
D200N
mutant shows no activation on light exposure
F197S
mutant shows no activation on light exposure
L111A/L115A
mutant shows no activation on light exposure
N256A
mutant shows no activation on light exposure
Y125A
mutant shows no activation on light exposure
D200N
-
mutant shows no activation on light exposure
-
F197S
-
mutant shows no activation on light exposure
-
L111A/L115A
-
mutant shows no activation on light exposure
-
N256A
-
mutant shows no activation on light exposure
-
Y125A
-
mutant shows no activation on light exposure
-
A197T
the mutant shows increased activity compared to the wild type enzyme
D212N
-
mutant with no detectable enzyme activity
D214N
-
mutant with no 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
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
K274A
-
the mutation significantly reduces adenylate cyclase activity
K81M
-
mutant with no detectable enzyme activity
K88I
-
mutant with no detectable enzyme activity
L326P
the mutant shows increased activity compared to the wild type enzyme
r23ExoY
-
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
T351A
-
the mutation significantly reduces adenylate cyclase 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
-
F399I
-
the mutant shows increased activity compared to the wild type enzyme
-
L326P
-
the mutant shows increased activity compared to the wild type enzyme
-
R318W
-
the mutant shows increased activity compared to the wild type enzyme
-
K274A
-
the mutation significantly reduces adenylate cyclase activity
-
T351A
-
the mutation significantly reduces adenylate cyclase activity
-
D396A
-
almost no activity
D396A/D440A
-
no activity
D396A/D440N
-
no activity
D396N
-
almost no activity
D396N/D440A
-
no activity
D396N/D440N
-
no activity
D425A
-
catalytically inactive mutant of isoform AC6, the expression of the mutant is associated with marked reduction in cAMP production
D440A
-
almost no activity
D440N
-
almost no activity
K1876M
-
large decrease in cAMP signalling
C83A
Q7CH76
the mutation results in moderate to sharp decreases in activity in the presence of 10 mM Mn2+ or 20 mM Mg2+
D143A
-
does not crystallize
D55K
Q7CH76
the mutant shows increased Km for Mg2+ compared to the wild type enzyme
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+
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+
E497K/C566D
mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclases
E497K/C566D
-
mutations within the nucleotide binding site generates rhodopsin-adenylyl cyclases
-
D365C
-
0.06% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
D365C
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
F363R
mutant with poor adenylate cyclase acitivity
F363R
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
K296E
-
0.5% of wild-type activity, mutant displays classical Michaelis-Menten kinetics, in contrast to the sigmoidal kinetics of the wild-type
K296E
mutant with about 400fold reduced enzyme activity
K296E
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
-
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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
O06362, O06572, O07732, O53213, O53720, P71914, P94982, P9WM05, P9WMU7, P9WMV1, P9WQ29, P9WQ31, P9WQ33, P9WQ35, Q11028 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
K296E
-
mutant with about 400fold reduced enzyme activity
-
K296E
-
Rv1625c mutant, does not result in a gain of guanylyl cyclase activity, but leads to severely compromised adenylyl cyclase activity
-
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
-
mutation of either His572 or Asp895 greatly reduces AC activity
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
-
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
-
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
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
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
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
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
additional information
-
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
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
additional information
-
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
additional information
-
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
additional information
-
deletion of a 12TM domain of ACA, does not perturb cAMP secretion
additional information
-
RNAi against gene AC78C, but not against gene ACXE, depressed the sucrose response in gustatory receptor neurons
additional information
-
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
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
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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
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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
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
additional information
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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
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
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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deletion of sAC, leads to inhibition of sperm mobility, animals are infertile, AC3 knockout mice, exhibit peripheral and behavioral anosmia
additional information
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homozygous mutants AC1KO, AC8KO and AC1/AC8KO
additional information
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knockout of sAC in mice causes male sterility by impaired sperm motility, while spermatogenesis is not affected
additional information
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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
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
additional information
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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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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
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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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
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
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 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 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 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
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 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 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
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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
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
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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
additional information
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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
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
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
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
additional information
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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
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
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
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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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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
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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
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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-/- 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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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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homozygous mutants AC1KO, AC8KO and AC1/AC8KO
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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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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 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
additional information
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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
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
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
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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
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additional information
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knock-out strain lacking Rv1625c is as virulent as the wild-type strain in the mouse model of tuberculosis infection
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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
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additional information
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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
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
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
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
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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
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disruption of a class IIIb AC gene results in strong attenuation
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
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
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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
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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
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strain lacking the Rv1264-like cyclase is unable to execute an apparently cAMP and acid pH-dependent differentiation pathway
additional information
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truncated version of Cya1 consisting of amino acids 95 to 338, mutant with significant lower specific activity
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analysis
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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
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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
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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
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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
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drug development
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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
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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
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AC1 is a potential drug target site to improve long-term remote memor
medicine
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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
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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
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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
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AC5 is the major AC isoform mediating acute beta-adrenergic stimulation, AC5 plays a major role in L-type Ca2+ currents activation
medicine
-
AC6 improves function in Galphaq-hypertrophic pigs
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
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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
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involved in mediating opioid actions, AC5 is essential for micro, and to a lesser extent, delta, opioid receptor signaling in striatum
medicine
-
overexpression of AC6 or drug-stimulated cAMP accumulation in WI-38 lung fibroblast attenuates fibrosis
medicine
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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
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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
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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
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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
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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
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involved in mediating opioid actions, AC5 is essential for micro, and to a lesser extent, delta, opioid receptor signaling in striatum
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medicine
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AC5 is the major AC isoform mediating acute beta-adrenergic stimulation, AC5 plays a major role in L-type Ca2+ currents activation
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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
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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
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pharmacology
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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
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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
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additional information
15 putative AC genes present
additional information
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AC8 acts as a low-pass filter for high-frequency Ca2+ events, enhancing the regulatory options available to this signalling pathway
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
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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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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
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both sAC and tmACs participate in the sperm acrosome reaction and sperm motility
additional information
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Ca2+-stimulated AC regulates If via cAMP, modulation of the If pacemaker current
additional information
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can function as a ion channel
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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compartmentalization of cAMP signalling, cAMP levels change in discrete domains of the cell with discrete local consequences
additional information
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contains a GGDEF domain
additional information
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaB1 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaB2 is composed of two GAF domains, a PAS domain, a CHD and a single tetratricopeptide repeat
additional information
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
CyaC consists of a receiver domain, two GAF domains, a histidine kinase domain, another receiver and a CHD
additional information
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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
Drosophila sp. (in: flies)
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essential role of Ca2+/calmodulin-regulated ACs in learning and memory
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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involved in sensing high osmotic pressure
additional information
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is an exotoxin
additional information
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is an exotoxin
additional information
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is an exotoxin
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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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
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overexpression of AC1 in forebrain enhances long-term potentiation
additional information
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restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
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restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
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restores adenylate cyclase activity in Escherichia coli knockout mutants
additional information
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restores adenylate cyclase activity in Escherichia coli knockout mutants
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
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
-
Rv1264 plays a role in mycobacterial survival in the acidic environment of the pahgolysosome
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1318c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1319c has a HAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
additional information
Rv1320c has aHAMP domain
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
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
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
-
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
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
additional information
Rv3645 has a HAMP domain
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
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senses ional changes in the environment
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
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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
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
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ACT enhances the adhesive functions of filamentous haemagglutinin and modifies the performance of the filamentous haemagglutinin heparin-inhibitable carbohydrate binding site
-
additional information
-
Rv0386 shows both adenylyl and a guanylyl cyclase side-activity
-
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
-
Rv1320c has aHAMP domain
-
additional information
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Rv1319c has a HAMP domain
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additional information
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Rv1318c has a HAMP domain
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additional information
-
15 putative AC genes present
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additional information
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Rv1625c has the highest sequence similarity with the mammalian enzymes
-
additional information
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ACIII is a marker for primary cilia throughout many regions of the adult mouse brain
-