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ATP + 40S-ribosomal protein S6
?
-
rat brain
-
-
?
ATP + a protein
ADP + a phosphoprotein
ATP + actin
ADP + phosphoactin
-
-
-
-
?
ATP + Akt
ADP + phosphorylated Akt
ATP + alpha-casein
ADP + phosphorylated alpha-casein
ATP + alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide
ADP + phosphorylated alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide
-
phosphorylated in vitro by CaMKII predominantly on the I-II linker
-
-
?
ATP + autocamtide-2
ADP + phosphorylated autocamtide-2
ATP + Bcl10
ADP + phosphorylated Bcl10
-
phosphorylation by CaMKII at Ser138, recombinant FLAG-tagged Bcl10 substrate expressed in HEK-293T cells
-
-
?
ATP + beta-Pak-interacting exchange factor
ADP + phosphorylated beta-Pak-interacting exchange factor
beta-Pak-interacting exchange factor is phosphorylated at Ser156
-
-
?
ATP + biotinylated Thr-Arg-Ser-Ala-Ile-Arg-Arg-Ala-Ser-Thr-Ile-Glu-Met-Pro-Gln-Gln-Ala-Arg-Gln
ADP + biotinylated Thr-Arg-Ser-Ala-Ile-Arg-Arg-Ala-Ser-phospho-Thr-Ile-Glu-Met-Pro-Gln-Gln-Ala-Arg-Gln
biotinylated phospholamban Thr17 peptide substrate
-
-
?
ATP + Blc10
ADP + phosphorylated Blc10
ATP + bovine serum albumin
ADP + phosphorylated bovine serum albumin
-
low activity
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase I
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase I
ATP + Ca2+/calmodulin-dependent protein kinase IV
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase IV
ATP + Cabin1
ADP + phosphorylated Cabin1
ATP + caldesmon
ADP + caldesmon phosphate
ATP + cAMP response element binding protein
ADP + phosphorylated cAMP response element binding protein
-
-
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
ATP + cAMP-response element-binding protein
ADP + phosphorylated cAMP-response element-binding protein
-
i.e. CREB, phosphorylation at S133, substrate of CaMKIV and CaMKII
-
-
?
ATP + cAMP-responsive element-binding protein
ADP + phosphorylated cAMP-responsive element-binding protein
ATP + CARMA1
ADP + phosphorylated CARMA1
ATP + casein
?
-
rat brain
-
-
?
ATP + casein
ADP + phosphocasein
ATP + casein
ADP + phosphorylated casein
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
ATP + CREB
ADP + phosphorylated CREB
ATP + CREB1 protein
ADP + phosphorylated CREB1 protein
-
-
-
?
ATP + cyclic AMP response element binding protein
ADP + phosphorylated cyclic AMP response element binding protein
-
phosphorylated at Ser133
-
-
?
ATP + dystrophin Dp71d
ADP + phosphorylated dystrophin Dp71d
ATP + Emi2
ADP + phosphorylated Emi2
an APC/C repressor, inactivation
-
-
?
ATP + estrogen-receptor from calf uterus
?
-
-
-
-
?
ATP + eukaryotic translation initiation factor 4B
ADP + phosphorylated eukaryotic translation initiation factor 4B
-
-
-
?
ATP + GABA A receptor
ADP + phosphorylated GABA A receptor
-
-
-
-
?
ATP + GABA-modulin
?
-
-
-
-
?
ATP + glutamate receptor subunit GluR1
ADP + phosphorylated glutamate receptor subunit GluR1
ATP + glutamate receptor subunit NR2B
ADP + phosphorylated glutamate receptor subunit NR2B
ATP + glycogen synthase
?
-
rat brain
-
-
?
ATP + glycogen synthase
ADP + phosphorylated glycogen synthase
-
-
-
-
?
ATP + glycosylated phosducin-like protein
ADP + glycosylated phosducin-like phosphoprotein
-
-
-
-
?
ATP + group I metabotropic glutamate receptor
ADP + phosphorylated group I metabotropic glutamate receptor
-
CaMKIV contributes to the upregulation of fragile X mental retardation protein induced by stimulating group I metabotropic glutamate receptors
-
-
?
ATP + GST-tagged GluN2A
ADP + phosphorylated GST-tagged GluN2A
-
-
-
-
?
ATP + GST-tagged GluN2B
ADP + phosphorylated GST-tagged GluN2B
-
-
-
-
?
ATP + histone
ADP + phosphohistone
ATP + histone deacetylase 4
ADP + phosphorylated histone deacetylase 4
ATP + histone deacetylase 5
ADP + phosphorylated histone deacetylase 5
ATP + histone H1
ADP + phosphorylated histone H1
rat CaMKIV prefers histone H1 over myelin basic protein, while Danio rerio CaMKIV does not
-
-
?
ATP + histone IIA
ADP + phosphorylated histone IIA
-
-
-
-
?
ATP + histone IIIS
ADP + phosphorylated histone IIIS
ATP + histone IIS
ADP + phosphorylated histone IIS
-
-
-
-
?
ATP + histone type IIA
ADP + phosphorylated histone type IIA
ATP + histone VI
ADP + phosphorylated histone VI
-
-
-
-
?
ATP + histone VIIS
ADP + phosphorylated histone VIIS
-
-
-
-
?
ATP + histone VIS
ADP + phosphorylated histone VIS
-
-
-
-
?
ATP + histone VS
ADP + phosphorylated histone VS
-
-
-
-
?
ATP + Homer3 protein
ADP + Homer3 phosphoprotein
-
Homer3 protein is phosphorylated at Ser120, Ser159, and Ser176 by CaMKII
-
-
?
ATP + human cardiac sodium channel NaV1.5
ADP + phosphorylated human cardiac sodium channel NaV1.5
ATP + I-kappaB
ADP + phosphorylated I-kappaB
ATP + Kemptide
ADP + LRRAS(P)LG
-
i.e. LRRASLG, low activity
-
-
?
ATP + Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ADP + phosphorylated Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ATP + KKALRRQETVDAL
ADP + KKALRRQET(P)VDAL
-
i.e. autocamtide-2
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
ATP + MAP2
ADP + phosphorylated MAP2
-
-
-
-
?
ATP + MEF-2A
ADP + phosphorylated MEF-2A
-
phosphorylation by CaMKIV
-
-
?
ATP + MEF-2C
ADP + phosphorylated MEF-2C
-
phosphorylation by CaMKIV
-
-
?
ATP + MEF-2D
ADP + phosphorylated MEF-2D
-
phosphorylation by CaMKIV
-
-
?
ATP + microtubule affinity regulating kinase 2
ADP + phosphorylated microtubule affinity regulating kinase 2
ATP + microtubule associated protein 2
ADP + phosphorylated microtubule associated protein 2
-
-
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
ATP + microtubule-associated protein tau
?
ATP + myelin basic protein
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
ATP + myosin
ADP + phosphomyosin
ATP + myosin II light chain
ADP + phosphorylated myosin II light chain
ATP + myosin light chain
?
ATP + myosin light chain
ADP + phosphorylated myosin light chain
ATP + Na+-channel
ADP + phosphorylated Na+-channel
ATP + NADPH oxidase 5
ADP + phosphoraletd NADPH oxidase 5
ATP + neuronal nitric-oxide synthase
ADP + phosphorylated neuronal nitric-oxide synthase
ATP + NFkappaB
ADP + phosphorylated NFkappaB
-
the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536
-
-
?
ATP + NHE-1
ADP + phosphorylated NHE-1
ATP + NMDA receptor
ADP + phosphorylated NMDA receptor
-
-
-
-
?
ATP + Notch1 protein
ADP + phosphorylated Notch1 protein
ATP + PC12 pheochromacytoma cell line protein substrate pp250
?
-
-
-
-
?
ATP + peptide AC2
ADP + phosphorylated peptides AC2
-
Ca2+-independent autonomous activity after Thr286 autophosphorylation is65% of maximal stimulated activity
-
-
?
ATP + phosphatidylinositol 3-kinase
ADP + phosphorylated phosphatidylinositol 3-kinase
-
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
ATP + phosvitin
ADP + phosphorylated phosvitin
-
-
-
-
?
ATP + PLB
ADP + phosphorylated PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + PLN
ADP + phosphorylated PLN
ATP + PLRRTLSVAA
ADP + ?
-
-
-
-
?
ATP + PLRRTLSVAA-amide
ADP + phosphorylated PLRRTLSVAA-amide
-
glycogen synthase-derived peptide GSP
-
-
?
ATP + protamin
ADP + phosphorylated protamin
-
low activity
-
-
?
ATP + protein
ADP + phosphoprotein
ATP + protein
ADP + phosphorylated protein
ATP + protein CREB
ADP + phosphorylated protein CREB
ATP + protein ERK
ADP + phosphorylated protein ERK
ATP + protein HDAC
ADP + phosphorylated protein HDAC
ATP + protein kinase B
ADP + phosphorylated protein kinase B
-
-
-
-
?
ATP + protein kinase G
ADP + phosphorylated protein kinase G
-
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
ATP + protein PLN
ADP + phosphorylated Pprotein LN
-
PLN regulation through phosphorylation by CaMKII at Thr17
-
-
?
ATP + protein PLN
ADP + phosphorylated protein PLN
-
a sarcoplasmic reticulum protein, phosphorylation by CaMKII at Thr17
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
ATP + PSD-95
ADP + phosphorylated PSD-95
ATP + Raf-1 protein
ADP + phosphorylated Raf-1 protein
ATP + ryanodine receptor type 2
ADP + phosphorylated ryanodine receptor type 2
ATP + RyR
ADP + phosphorylated RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + S6-kinase
?
-
step of a protein kinase cascade initiated by insulin in a yet unidentified manner
-
-
?
ATP + Stargazin
ADP + phosphorylated Stargazin
ATP + STAT3
ADP + phosphorylated STAT3
-
-
-
?
ATP + stress-induced phosphoprotein 1
ADP + phosphorylated stress-induced phosphoprotein 1
phosphorylated on Ser198
-
-
?
ATP + synapsin
?
-
rat brain
-
-
?
ATP + synapsin
ADP + phosphorylated synapsin
-
-
-
-
?
ATP + synapsin
ADP + phosphosynapsin
ATP + synapsin I
ADP + phosphorylated synapsin I
ATP + synapsin I
ADP + phosphosynapsin I
-
-
-
?
ATP + synapsin II
ADP + phosphorylated synapsin II
ATP + synapsin-1
ADP + phopshorylated synapsin-1
-
-
-
-
?
ATP + synGAP
ADP + phosphorylated synGAP
ATP + syntide-2
ADP + phosphorylated syntide-2
ATP + syntide-2 peptide
phosphorlyated syntide-2 peptide
syntide-2 peptide is L-prolyl-L-leucyl-L-alanyl-L-arginyl-L-threonyl-L-leucyl-L-seryl-L-valyl-L-alanylglycyl-L-leucyl-L-prolylglycyl-L-lysyl-L-lysine
-
-
?
ATP + syntide2
ADP + phosphorylated syntide2
-
Ca2+-independent autonomous activity after Thr286 autophosphorylation is25% of maximal stimulated activity
-
-
?
ATP + tau peptide 408-420
ADP + phosphorylated tau peptide 408-420
ATP + tau protein
ADP + phosphorylated tau protein
ATP + tropomyosin
ADP + phosphotropomyosin
-
-
-
-
?
ATP + type alpha cytosolic phospholipase A2
ADP + phosphorylated type alpha cytosolic phospholipase A2
-
CaMK regulates the type alpha cytosolic phospholipase A2 via phosphorylation at Ser515
-
-
?
ATP + vimentin
?
-
rat brain
-
-
?
ATP + vimentin
ADP + phosphorylated vimentin
ATP + voltage-gated calcium channel beta1b subunit
ADP + phosphorylated voltage-gated calcium channel beta1b subunit
-
-
-
?
ATP + voltage-gated calcium channel beta2a subunit
ADP + phosphorylated voltage-gated calcium channel beta2a subunit
CaMKII phosphorylates at Thr498
-
-
?
ATP + voltage-gated calcium channel beta3 subunit
ADP + phosphorylated voltage-gated calcium channel beta3 subunit
-
-
-
?
ATP + voltage-gated calcium channel beta4 subunit
ADP + phosphorylated voltage-gated calcium channel beta4 subunit
-
-
-
?
ATP + YLRRRLSDSNF
ADP + ?
synapsin site I-derived peptide substrate
-
-
?
additional information
?
-
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
the enzyme phosphorylates e.g. the synaptic vesicle-associated protein synapsin 1 and synapsin 2
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
substrate of CaM-KII, phosphorylation at Thr308
-
-
?
ATP + Akt
ADP + phosphorylated Akt
the enzyme (CaMKK2) directly phosphorylates Akt at Thr308
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
substrate of CaM-KII, phosphorylation at Thr308
-
-
?
ATP + Akt
ADP + phosphorylated Akt
-
substrate of CaM-KII, phosphorylation at Thr308
-
-
?
ATP + alpha-casein
ADP + phosphorylated alpha-casein
-
-
-
?
ATP + alpha-casein
ADP + phosphorylated alpha-casein
-
-
-
?
ATP + autocamtide-2
ADP + phosphorylated autocamtide-2
highly selective peptide substrate for calcium/calmodulin-dependent protein kinase II
-
-
?
ATP + autocamtide-2
ADP + phosphorylated autocamtide-2
-
substrate in activity assay
-
-
?
ATP + autocamtide-2
ADP + phosphorylated autocamtide-2
highly selective peptide substrate for calcium/calmodulin-dependent protein kinase II
-
-
?
ATP + Blc10
ADP + phosphorylated Blc10
-
activation
-
-
?
ATP + Blc10
ADP + phosphorylated Blc10
-
Bcl10 is essential for antigen receptor-induced NF-kappaB activation, interleukin-2 production, and T-cell proliferation but is not required for TCR-induced tyrosine phosphorylation, calcium flux, or extracellular signal-regulated kinase activation
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase I
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase I
-
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase I
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase I
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation. Ca2+/calmodulin-dependent protein kinase kinase phosphorylates and activates Ca2+/calmodulin-dependent protein kinase I and Ca2+/calmodulin-dependent protein kinase IV, which directly activate transcription factors
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase IV
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase IV
-
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase IV
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase IV
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation. Ca2+/calmodulin-dependent protein kinase kinase phosphorylates and activates Ca2+/calmodulin-dependent protein kinase I and Ca2+/calmodulin-dependent protein kinase IV, which directly activate transcription factors
-
-
?
ATP + Cabin1
ADP + phosphorylated Cabin1
-
a transcriptional corepressor of myocyte enhancer factor 2, phosphorylation by CaMKIV creates a docking site for protein 14-3-3, which causes nuclear export, CaMKIV regulates nuclear export of Cabin1 during Ca2+-dependent T-cell activation, regulation overview
-
-
?
ATP + Cabin1
ADP + phosphorylated Cabin1
-
a transcriptional corepressor of myocyte enhancer factor 2, phosphorylation at Ser2126 by CaMKIV creates a docking site for protein 14-3-3, which causes nuclear export, no activity with Cabin1 mutant S2126A
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
r
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
r
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
r
ATP + caldesmon
ADP + caldesmon phosphate
-
less efficient than synapsin
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
caldesmon plays a role in the regulation of smooth muscle contraction
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
caldesmon plays a role in the regulation of smooth muscle contraction
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
phosphorylated at 82% the rate of casein
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
-
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
CaMKIV activates CREB by phosphorylation and stimulates CREB-mediated transcription
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
i.e. CREB
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
i.e. CREB, phosphorylation by CaMK II at Ser133
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-responsive element-binding protein
ADP + phosphorylated cAMP-responsive element-binding protein
-
i.e. CREB, CaM kinase II, as part of the Ca2+ and CaMK signaling cascade, regulates the phosphorylation of CREB of spinal cord in rats following noxious stimulation, e.g. by capsaicin injection
-
-
?
ATP + cAMP-responsive element-binding protein
ADP + phosphorylated cAMP-responsive element-binding protein
-
i.e. CREB, phosphorylation at Ser133
-
-
?
ATP + CARMA1
ADP + phosphorylated CARMA1
-
CaMKII is a modulator of CARMA1-mediated NF-kappaB activation, overview
-
-
?
ATP + CARMA1
ADP + phosphorylated CARMA1
-
activation by phosphorylation at Ser109, interaction with Bcl10 is facilitated
-
-
?
ATP + casein
ADP + phosphocasein
-
-
-
-
?
ATP + casein
ADP + phosphocasein
-
phosphorylation at about 60% the rate of caldesmon
-
-
?
ATP + casein
ADP + phosphocasein
-
best substrate
-
-
?
ATP + casein
ADP + phosphorylated casein
-
low activity
-
-
?
ATP + casein
ADP + phosphorylated casein
-
-
-
-
?
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
in inner retina, isoform CaMKII-delta colocalizes with connexin36 protein
-
-
?
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
in the outer and inner retina, isoform CaMKII-beta colocalizes with connexin36-containing gap junctions
-
-
?
ATP + CREB
ADP + phosphorylated CREB
-
i.e. cAMP-response element binding protein, substrate of CaM-KI, phosphorylation at Ser133
-
-
?
ATP + CREB
ADP + phosphorylated CREB
-
i.e. cAMP-response element binding protein, substrate of CaM-KI, phosphorylation at Ser133
-
-
?
ATP + CREB
ADP + phosphorylated CREB
-
i.e. cAMP-response element binding protein, substrate of CaM-KI, phosphorylation at Ser133
-
-
?
ATP + dystrophin Dp71d
ADP + phosphorylated dystrophin Dp71d
-
the phosphorylation process involves protein kinase C, EC 2.7.11.13, CAMKII-mediated phosphorylation modulates the Dp71 nuclear localization
-
-
?
ATP + dystrophin Dp71d
ADP + phosphorylated dystrophin Dp71d
-
a nuclear splicing isoform of Dp71, several potential sites for phosphorylation
-
-
?
ATP + glutamate receptor subunit GluR1
ADP + phosphorylated glutamate receptor subunit GluR1
-
low activity, CaMKII, membrane localization of GluR1 restricts its phosphorylation
-
-
?
ATP + glutamate receptor subunit GluR1
ADP + phosphorylated glutamate receptor subunit GluR1
-
phosphorylation at Ser831
-
-
?
ATP + glutamate receptor subunit NR2B
ADP + phosphorylated glutamate receptor subunit NR2B
-
-
-
-
?
ATP + glutamate receptor subunit NR2B
ADP + phosphorylated glutamate receptor subunit NR2B
-
low activity, CaMKII
-
-
?
ATP + histone
?
-
H1 (best substrate)
-
-
?
ATP + histone
?
-
H2a or H2b
-
-
?
ATP + histone
?
-
H1 (best substrate)
-
-
?
ATP + histone
?
-
V-S
-
-
?
ATP + histone
?
-
5S, 6S, 7S
-
-
?
ATP + histone
?
-
3S
-
-
?
ATP + histone
?
-
8S
-
-
?
ATP + histone
?
-
not: 2AS
-
-
?
ATP + histone
ADP + phosphohistone
-
histone V-S
-
-
?
ATP + histone
ADP + phosphohistone
-
histone III-S
-
-
?
ATP + histone
ADP + phosphohistone
-
calf thymus histone II-S, poor substrate
-
-
?
ATP + histone
ADP + phosphohistone
-
histone III-S
-
-
?
ATP + histone
ADP + phosphohistone
-
histone III-S
-
-
?
ATP + histone deacetylase 4
ADP + phosphorylated histone deacetylase 4
-
-
-
-
?
ATP + histone deacetylase 4
ADP + phosphorylated histone deacetylase 4
-
the enzyme may facilitate transcription factor activities by the neutralization of histone deacetylase 4 by phosphorylation, which may contribute to the phenotypic plasticity of gastrointestinal smooth muscle cells
-
-
?
ATP + histone deacetylase 5
ADP + phosphorylated histone deacetylase 5
-
-
-
?
ATP + histone deacetylase 5
ADP + phosphorylated histone deacetylase 5
-
whereas histone deacetylase 5 alone is unresponsive to CaMKII, it becomes responsive to CaMKII in the presence of histone deacetylase 4
-
-
?
ATP + histone deacetylase 5
ADP + phosphorylated histone deacetylase 5
-
-
-
?
ATP + histone IIIS
ADP + phosphorylated histone IIIS
-
-
-
-
?
ATP + histone IIIS
ADP + phosphorylated histone IIIS
-
-
-
?
ATP + histone type IIA
ADP + phosphorylated histone type IIA
-
-
-
?
ATP + histone type IIA
ADP + phosphorylated histone type IIA
-
-
-
?
ATP + human cardiac sodium channel NaV1.5
ADP + phosphorylated human cardiac sodium channel NaV1.5
-
the intracellular loop between domains 1 and 2 of cardiac sodium channel NaV1.5 is phosphorylated specifically at the Ser516 and Thr594 sites. The phosphorylation status of Ser516 and Thr594 on cardiac sodium channel NaV1.5, is an important mediator of the enzyme-dependent negative shift in cardiac sodium channel NaV1.5
-
-
?
ATP + human cardiac sodium channel NaV1.5
ADP + phosphorylated human cardiac sodium channel NaV1.5
-
the intracellular loop between domains 1 and 2 of cardiac sodium channel NaV1.5 is phosphorylated specifically at the Ser516 and Thr594 sites
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII
-
-
?
ATP + Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ADP + phosphorylated Kir6.2 subunit of cardiac ATP-sensitive potassium channel
-
-
-
-
?
ATP + Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ADP + phosphorylated Kir6.2 subunit of cardiac ATP-sensitive potassium channel
-
phosphorylation of Kir6.2 subunit of cardiac ATP-sensitive potassium channel promotes endocytosis of cardiac ATP-sensitive potassium channels
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation by CaMKII
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation by CaMKII
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation by CaMKII
-
-
?
ATP + microtubule affinity regulating kinase 2
ADP + phosphorylated microtubule affinity regulating kinase 2
-
CaMKIalpha/microtubule affinity regulating kinase 2 signaling cascade mediates calcium-dependent neurite outgrowth/axonal extension
-
-
?
ATP + microtubule affinity regulating kinase 2
ADP + phosphorylated microtubule affinity regulating kinase 2
-
i.e. MARK2, recombinant myc-tagged MARK2 expressed in HEK-293 cells, mutational determination of phosphorylation sites, overview
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
-
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
as good as myelin basic protein
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
rat brain: broad specificity
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
ATP preferred to GTP
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
not MAP-1
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
phosphorylation sites are serine and threonine
-
-
?
ATP + microtubule-associated protein 2
ADP + microtubule-associated protein 2 phosphate
-
i.e. MAP-2, preferred substrate
-
-
?
ATP + microtubule-associated protein tau
?
-
-
-
-
?
ATP + microtubule-associated protein tau
?
-
Ca2+/calmodulin dependent autophosphorylation
-
-
?
ATP + microtubule-associated protein tau
?
-
all 4 tau-species, but about 50% of tau1 and tau2 protein remains resistant to phosphorylation
-
-
?
ATP + microtubule-associated protein tau
?
-
-
-
-
?
ATP + microtubule-associated protein tau
?
-
Ca2+/calmodulin dependent autophosphorylation
-
-
?
ATP + microtubule-associated protein tau
?
-
all 4 tau-species, but about 50% of tau1 and tau2 protein remains resistant to phosphorylation
-
-
?
ATP + myelin basic protein
?
-
-
-
-
?
ATP + myelin basic protein
?
-
best substrate
-
-
?
ATP + myelin basic protein
?
-
phosphorylation sites: serine
-
-
?
ATP + myelin basic protein
?
-
phosphorylation sites: threonine
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
modest activity
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
modest activity
-
-
?
ATP + myelin basic protein
ADP + phosphorylated myelin basic protein
rat CaMKIV prefers histone H1 over myelin basic protein, while Danio rerio CaMKIV does not
-
-
?
ATP + myosin
ADP + phosphomyosin
-
-
-
-
?
ATP + myosin
ADP + phosphomyosin
-
isolated light chain of smooth-muscle myosin, phosphorylated at 80% the rate of caldesmon
-
-
?
ATP + myosin
ADP + phosphomyosin
-
-
-
-
?
ATP + myosin II light chain
ADP + phosphorylated myosin II light chain
recombinant substrate from Physarum polycephalum, phosphorylation at Ser18, phosphorylation site analysis, no phosphorylation of substrate mutant S18A
-
-
?
ATP + myosin II light chain
ADP + phosphorylated myosin II light chain
recombinant substrate from Physarum polycephalum, phosphorylation at Ser18, phosphorylation site analysis, no phosphorylation of substrate mutant S18A
-
-
?
ATP + myosin light chain
?
-
poor
-
-
?
ATP + myosin light chain
?
-
smooth-muscle, myosin, rat brain
-
-
?
ATP + myosin light chain
?
-
smooth-muscle, cardiac
-
-
?
ATP + myosin light chain
?
-
smooth-muscle, skeletal muscle
-
-
?
ATP + myosin light chain
ADP + phosphorylated myosin light chain
modest activity
-
-
?
ATP + myosin light chain
ADP + phosphorylated myosin light chain
modest activity
-
-
?
ATP + Na+-channel
ADP + phosphorylated Na+-channel
-
-
-
-
?
ATP + Na+-channel
ADP + phosphorylated Na+-channel
-
isozyme CaMKIIdelta increases persistent/late inward INa and intracellular Na+ concentration regulazing Na+ channel activity, CaMKII expression is increased in heart failure and may be involved in Na+ channel regulation alterations via calmodulin, overview
-
-
?
ATP + NADPH oxidase 5
ADP + phosphoraletd NADPH oxidase 5
-
the enzyme mediates the phosphorylation and activation of NADPH oxidase 5. The ability of Ca2+/calmodulin-dependent protein kinase to regulate NADPH oxidase 5 activity may be significant in the regulation of production of reactive oxygen species that occurs downstream of calcium-mobilizing agonists such as angiotensin II. Of these phosphorylation sites, mutation of only Ser475 to alanine prevents Ca2+/calmodulin-dependent protein kinase-induced increases in activity of NADPH oxidase 5
-
-
?
ATP + NADPH oxidase 5
ADP + phosphoraletd NADPH oxidase 5
-
phosphorylation on Thr494, Ser498, Ser475, Ser502, and Ser675
-
-
?
ATP + neuronal nitric-oxide synthase
ADP + phosphorylated neuronal nitric-oxide synthase
-
phosphorylation at Ser741 by CaM-K Ialpha, wild-type and truncation mutant 1-293 inhibits neuronal nitric-oxide synthase, nNOS, no substrate of CaM-K IIalpha and CaM-K IV
-
-
?
ATP + neuronal nitric-oxide synthase
ADP + phosphorylated neuronal nitric-oxide synthase
-
phosphorylation at Ser741 by CaM-K Ialpha, wild-type and truncation mutant 1-293 inhibits neuronal nitric-oxide synthase, nNOS, no substrate of CaM-K IIalpha and CaM-K IV, determination of phosphorylation sites by analytical SDS-PAGE
-
-
?
ATP + NHE-1
ADP + phosphorylated NHE-1
-
phosphorylation by CaMKII is regulated by phosphatase PP1 which is associated with the exchanger
-
-
?
ATP + NHE-1
ADP + phosphorylated NHE-1
-
a Na+-H+-exchanging protein, phosphorylation by CaMKII at the intracellular cytoplasmic domain
-
-
?
ATP + Notch1 protein
ADP + phosphorylated Notch1 protein
-
-
-
?
ATP + Notch1 protein
ADP + phosphorylated Notch1 protein
phosphorylation of Notch1 intracellular domain inhibits the proteasomal degradation of Notch1 intracellular domain through Fbw7 ubiquitin-protein ligase complex. Upregulated Notch1 intracellular domain accelerates osteoclast differentiation
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation by CaMKII activates the sarcoplasmic reticulum Ca2+-ATPase, increasing both the rate of Ca2+ clearance from the myoplasm and the frequency of localized Ca2+ release events from intracellular stores
-
-
?
ATP + PLN
ADP + phosphorylated PLN
-
phosphorylation contributes to mechanical recovery from acidosis by inhibiting SERCA2a inhibition
-
-
?
ATP + PLN
ADP + phosphorylated PLN
-
a sarcoplasmic reticulum protein, phosphorylation by CaMKII at Thr17
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation at Thr177
-
-
?
ATP + protein
ADP + phosphoprotein
autophosphorylation of Ca2+/calmodulin-dependent protein kinase II converts the enzyme to a Ca2+-independent form, autophosphorylation site is Thr286 in the alpha subunit
-
-
?
ATP + protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
activation by phosphorylation
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
-
the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
activation by phosphorylation
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
-
CaMKII regulates the phosphorylation of CREB in NMDA-induced retinal neurotoxicity
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
-
i.e. cyclic AMP-response element binding protein
-
-
?
ATP + protein ERK
ADP + phosphorylated protein ERK
activation by phosphorylation
-
-
?
ATP + protein ERK
ADP + phosphorylated protein ERK
activation by phosphorylation
-
-
?
ATP + protein HDAC
ADP + phosphorylated protein HDAC
-
phosphorylation by nuclear CaMKII results in HDAC translocation from nucleus to cytoplasm
-
-
?
ATP + protein HDAC
ADP + phosphorylated protein HDAC
-
nuclear CaMKII
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + PSD-95
ADP + phosphorylated PSD-95
-
high activity, CaMKII, smaller synapses show greater variability in PSD-95 phosphorylation
-
-
?
ATP + PSD-95
ADP + phosphorylated PSD-95
-
a protein implicated in the scaffolding and trafficking of AMPA receptors
-
-
?
ATP + Raf-1 protein
ADP + phosphorylated Raf-1 protein
-
-
-
-
?
ATP + Raf-1 protein
ADP + phosphorylated Raf-1 protein
-
the enzyme phosphorylates Raf-1 at Ser338 and mediates Ras-stimulated Raf-1 activation
-
-
?
ATP + ryanodine receptor type 2
ADP + phosphorylated ryanodine receptor type 2
-
i.e. RyR2
-
-
?
ATP + ryanodine receptor type 2
ADP + phosphorylated ryanodine receptor type 2
-
-
-
-
?
ATP + S6-kinase II
?
-
phosphorylation sites: serine and threonine
-
-
?
ATP + S6-kinase II
?
-
phosphorylation sites: serine and threonine
-
-
?
ATP + Stargazin
ADP + phosphorylated Stargazin
-
high activity, CaMKII, phosphatases limit phosphorylation of stargazin
-
-
?
ATP + Stargazin
ADP + phosphorylated Stargazin
-
a protein implicated in the scaffolding and trafficking of AMPA receptors
-
-
?
ATP + synapsin
ADP + phosphosynapsin
-
-
-
-
?
ATP + synapsin
ADP + phosphosynapsin
-
brain synapsin best substrate of chicken gizzard caldesmon kinase
-
-
?
ATP + synapsin
ADP + phosphosynapsin
-
brain synapsin best substrate, phosphorylated at 950% the rate of caldesmon
-
-
?
ATP + synapsin I
ADP + phosphorylated synapsin I
-
substrate of CaM-KI
-
-
?
ATP + synapsin I
ADP + phosphorylated synapsin I
-
substrate of CaM-KI
-
-
?
ATP + synapsin I
ADP + phosphorylated synapsin I
-
substrate of CaM-KI
-
-
?
ATP + synapsin II
ADP + phosphorylated synapsin II
-
substrate of CaM-KI
-
-
?
ATP + synapsin II
ADP + phosphorylated synapsin II
-
substrate of CaM-KI
-
-
?
ATP + synapsin II
ADP + phosphorylated synapsin II
-
substrate of CaM-KI
-
-
?
ATP + synGAP
ADP + phosphorylated synGAP
-
regulation and activation of the neuron-specific Ras GTPase-activating protein, synGAP, by phosphorylation through CaMKII in the postsynaptic density fraction of the forebrain, synGAP is part of the signaling complex attached to the cytoplasmic tail of the N-methyl-D-aspartate-type glutamate receptor, overview
-
-
?
ATP + synGAP
ADP + phosphorylated synGAP
-
activation of the neuron-specific Ras GTPase-activating protein, synGAP, by phosphorylation through CaMKII at Ser1123, Ser1058, Ser750, Ser751, Ser756, Ser764, and Ser/65, reduced activity with synGAP serines phosphorylation site mutants, determination of phosphorylation sites by mass spectrometry, overview
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
a peptide containing the R-X-X-S/T consensus phosphorylation site 2 of glycogen synthase within the sequence
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
-
i.e. PLARTLSVAGLPGKK
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
-
-
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
-
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
-
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
a peptide containing the R-X-X-S/T consensus phosphorylation site 2 of glycogen synthase within the sequence
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
i.e. PLARTLSVAGLPGKK, synthetic peptide substrate
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
a peptide substrate
-
-
?
ATP + syntide-2
ADP + phosphorylated syntide-2
i.e. PLARTLSVAGLPGKK
-
-
?
ATP + tau peptide 408-420
ADP + phosphorylated tau peptide 408-420
-
recombinant substrate expressed in Escherichia coli, phosphorylation at Ser416 by CaM kinase II, no activity with the peptide by CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
-
-
?
ATP + tau peptide 408-420
ADP + phosphorylated tau peptide 408-420
-
recombinant substrate expressed in Escherichia coli, phosphorylation at Ser416 by CaM kinase II, no activity with the peptide by CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development, CaM kinase II is involved in the accumulation of tau in neuronal soma in Alzheimer's disease brain
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
recombinant substrate expressed in Escherichia coli, determination of phosphorylation sites, phosphorylation at Ser416 by CaM kinase II, tau is also a substrate for CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
recombinant substrate expressed in Escherichia coli, determination of phosphorylation sites, phosphorylation at Ser416 by CaM kinase II, tau is also a substrate for CDK5, EC 2.7.11.22, and casein kinase II, EC 2.7.11.26
-
-
?
ATP + tubulin
?
-
-
-
-
?
ATP + tubulin
?
-
rat brain
-
-
?
ATP + vimentin
ADP + phosphorylated vimentin
-
specific phosphorylation by CaMKII at Ser82
-
-
?
ATP + vimentin
ADP + phosphorylated vimentin
-
specific phosphorylation by CaMKII at Ser82, wild-type vimentin protein and a construct of a vimentin peptide containing Ser82 fused to the NMDA receptor 2B subunit, an interaction partner of CaMKII
-
-
?
additional information
?
-
-
the enzyme performs Ca2+/calmodulin-dependent autophosphorylation at a Ser residue
-
-
?
additional information
?
-
-
CaMKII induces changes of Na+ channel gating
-
-
?
additional information
?
-
the C-terminal region of rat CaMKIV, which is absent from Danio rerio CaMKIV, is involved in the regulation of both its substrate specificity and its susceptibility to dephosphorylation by nuclear CaMK phosphatase
-
-
?
additional information
?
-
-
the C-terminal region of rat CaMKIV, which is absent from Danio rerio CaMKIV, is involved in the regulation of both its substrate specificity and its susceptibility to dephosphorylation by nuclear CaMK phosphatase
-
-
?
additional information
?
-
involved in neuroplasticity. Mutant caki flies show reduced walking speed in 'Buridan's paradigm'
-
-
?
additional information
?
-
-
CaM kinase II plays a role in diverse cellular processes, overview
-
-
?
additional information
?
-
-
CaMKII is crucial for cellular and behavioral plasticity, autophosphorylation renders the enzyme independent on Ca2+ and calmodulin, which allows it to act as a molecular memory switch, CaMKII is required for memory formation of the brain in specific neurons, Ca2+-independent CaMKII mutant T287D in the adult Drosophila melanogaster CNS enhances plasticity and the training of pheromonal cues, mechanism, overview
-
-
?
additional information
?
-
-
CaM kinase II is strongly phosphorylated by protein kinase A PKA, EC 2.7.11.11, in electrocyte membranes, the activated CaM kinase II 2fold activates the Ca2+ pump and ATPase in the membranes, overview
-
-
?
additional information
?
-
-
substrate specificity
-
-
?
additional information
?
-
-
protein kinases and protein phosphatases regulate enzyme activities in the cell, overview
-
-
?
additional information
?
-
-
the enzyme prefers lysine-rich substrates, no activity with phosvitin and bovine serum albumin, the enzyme performs strictly Ca2+-dependent autophosphorylation which is influenced by substrates, overview
-
-
?
additional information
?
-
-
-
-
-
?
additional information
?
-
-
no substrates are bovine cardiac C-protein, bovine brain fodrin, rabbit skeletal muscle glycogen synthase, phosphorylase B, troponon (I + T + C), actin, tropomyosin, smooth muscle actin, filamin, vinculin, alpha-actinin, protamine or phosvitin
-
-
?
additional information
?
-
-
caldesmon is not a substrate of smooth-muscle myosin light-chain kinase
-
-
?
additional information
?
-
-
isozyme of calmodulin-dependent multifunctional protein kinase II in smooth-muscle
-
-
?
additional information
?
-
-
Ca2+ signaling in T-cell activation involves transcriptional activity of MEF-2 and NFAT, which is repressed by Cabin1, activated CaMKIV can overcome the repression by Cabin1, crosstalk between Cabin1 and CaMKIV, dissociation of Cabin1 from MEF-2 by the enzyme requires calmodulin, overview
-
-
?
additional information
?
-
CaM-KI and calcium/calmodulin-dependent kinase kinase CaM-KK participate in the control of cell cycle progression in MCF-7 human breast cancer cells, CaM-KK controls the G0-G1 restriction check point
-
-
?
additional information
?
-
-
CaM-KI and calcium/calmodulin-dependent kinase kinase CaM-KK participate in the control of cell cycle progression in MCF-7 human breast cancer cells, CaM-KK controls the G0-G1 restriction check point
-
-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy, CaMKIIdeltaB expression is increased in heart failure, about 2fold in failing cardiomyopathy, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
components of the Ca2+/calmodulin-dependent protein kinase cascade, overview
-
-
?
additional information
?
-
-
the enzyme is regulated by Ca2+/calmodulin binding and reversible phosphorylation, overview, the autonomous, Ca2+/calmodulin-independent activity of autophosphorylated Ca2+/calmodulin-dependent protein kinase IV is required for its role in transcription
-
-
?
additional information
?
-
CaM-K1delta performs autophosphorylation in a Ca2+/calmodulin-dependent manner which has no impact on its kinase activity
-
-
?
additional information
?
-
-
CaMKII is a multifunctional enzyme
-
-
?
additional information
?
-
-
CaMKII is a major component of the postsynaptic density of excitatory synapses, and plays a key role in the regulation of synaptic function in the mammalian brain, the unique molecular architecture of the postsynaptic density results in highly selective substrate discrimination by CaMKII, overview
-
-
?
additional information
?
-
-
CaMKII substrates CARMA1 and Bcl10 functionally interact and control NF-kappaB signaling downstream of the T-cell receptor
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
-
-
?
additional information
?
-
-
CaMKII performs autophosphorylation, and may also regulate Na+ channels, overview
-
-
?
additional information
?
-
-
CaMKII regulates P/Q-type Ca2+ current in neurons
-
-
?
additional information
?
-
CaMKIIgamma is activated by autophosphorylation
-
-
?
additional information
?
-
-
isozyme CaMKI is activated upon phosphorylation by CaMK kinase on Thr-177 located in activation loop
-
-
?
additional information
?
-
isozyme CaMKI is activated upon phosphorylation by CaMK kinase on Thr-177 located in activation loop
-
-
?
additional information
?
-
isozyme CaMKI is activated upon phosphorylation by CaMK kinase on Thr-177 located in activation loop
-
-
?
additional information
?
-
-
isozyme CaMKII is activated upon autophosphorylation on Thr-286 located in autoinhibitory domain
-
-
?
additional information
?
-
isozyme CaMKII is activated upon autophosphorylation on Thr-286 located in autoinhibitory domain
-
-
?
additional information
?
-
isozyme CaMKII is activated upon autophosphorylation on Thr-286 located in autoinhibitory domain
-
-
?
additional information
?
-
-
isozyme CaMKIV is activated upon phosphorylation by CaMK kinase on Thr-196 located in activation loop
-
-
?
additional information
?
-
isozyme CaMKIV is activated upon phosphorylation by CaMK kinase on Thr-196 located in activation loop
-
-
?
additional information
?
-
isozyme CaMKIV is activated upon phosphorylation by CaMK kinase on Thr-196 located in activation loop
-
-
?
additional information
?
-
-
CaMKII binds directly to a site in the C-terminal domain of CaV2.1 channels, autophosphorylation of CaMKII stimulates binding to this site. Autophosphorylated CaMKII can bind to the CaV2.1 channel and synapsin-1 simultaneously. Binding of CaV2.1 to CaMKII induces Ca2+-independent kinase activity, which mediates both autophosphorylation and phosphorylation of synapsin-1 at Ser603. Binding of autophosphorylated CaMKII to GST-tagged CaV2.1(18481964) is substantially greater than binding of nonactivated CaMKII. CaM is not required for CaMKII binding to Ca2+channels. Binding of autophosphorylated CaMKII persists after Ca2+/CaM dissociation
-
-
?
additional information
?
-
-
substrate specificity and binding structure, the enzyme depends on basic residues for substrate recognition, autoregulation by a pseudosubstrate mechanism, overview
-
-
?
additional information
?
-
-
the enzyme performs autophosphorylation
-
-
?
additional information
?
-
-
calmodulin-dependent kinase kinase/calmodulin kinase I activity, not CaMKIV or CaMKII, gates extracellular-signal-regulated kinase-dependent long-term potentiation required for learning and memory, Ras-GRF1 and ERK are also involved, NMDA-dependent activation of ERK, CaMKK pathway regulation, overview
-
-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
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-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
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-
?
additional information
?
-
-
CaMKII is required for gene transcription induced in the hippocampus by contextual fear conditioning, alphaCaMKII autophosphorylation is required for memory consolidation-specific transcription and formation of long term potentiation and memory, molecular mechanism, overview
-
-
?
additional information
?
-
-
CaMKIV regulation, overview, CaMKIV functions as a potent stimulator of Ca2+-dependent gene expression
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
CaMKII is a multifunctional enzyme
-
-
?
additional information
?
-
-
CaMKII performs autophosphorylation
-
-
?
additional information
?
-
-
isozyme-selective CaMKII binding sequence for interaction with ligand proteins, overview
-
-
?
additional information
?
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
-
CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview
-
-
?
additional information
?
-
-
CaMKII is critical in regulating myocyte function with regard to excitation-contraction-relaxation cycles and excitation-transcription coupling
-
-
?
additional information
?
-
-
CaMKII isozymes have distinct cellular localizations and function, overview, release of acetylcholine from dual transmitting sympathetic neurons requires activation of both the p75 receptor and activated CaMKII, model for neurotrophin-dependent modulation of cholinergic transmission, neurotrophins can influence CaMKII signaling by regulating the production of CaMKII protein and/or by changing the level of CaMKII activation, overview
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
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-
?
additional information
?
-
-
the enzyme is involved in dendritogenesis in cortical neurons and is required for brain-derived neurotropic factor-stimulated dendritic growth, and regulation of dendritic morphogenesis via the lipid-raft-delineated CL3-STEF-RAc pathway contributing to the development of cortical dendrites, overview
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-
?
additional information
?
-
-
CaMKII performs autophosphorylation, and may also regulate Na+ channels, overview
-
-
?
additional information
?
-
-
generation of Ca2+-independent activity after Thr286 autophosphorylation is a vital step in regulating synaptic plasticity and learning and memory. The autonomy is substrate-dependent, and low autonomy (15-25%) is the general default
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-
?
additional information
?
-
-
generation of Ca2+-independent autonomous activity by Thr286 autophosphorylation
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-
?
additional information
?
-
in terms of substrate specificity, the consensus sequences for phosphorylation by CaMKI, CaMKII, and CaMKIV are quite similar, and hence these kinases sometimes phosphorylate the same substrates, for example cAMP-response element-binding protein. Expression of Camk2g and Camk2d, but not Camk1 or Camk4, in Camk2g-/- eggs leads to degradation of exogenously expressed EMI2
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-
?
additional information
?
-
-
in terms of substrate specificity, the consensus sequences for phosphorylation by CaMKI, CaMKII, and CaMKIV are quite similar, and hence these kinases sometimes phosphorylate the same substrates, for example cAMP-response element-binding protein. Expression of Camk2g and Camk2d, but not Camk1 or Camk4, in Camk2g-/- eggs leads to degradation of exogenously expressed EMI2
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-
?
additional information
?
-
CaMKIIgamma possesses an intrinsic autophosphorylating activity, which renders the enzyme insensitive to changes in intracellular Ca2+ level
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-
?
additional information
?
-
-
CaMKIIgamma possesses an intrinsic autophosphorylating activity, which renders the enzyme insensitive to changes in intracellular Ca2+ level
-
-
?
additional information
?
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
the enzyme performs Ca2+/calmodulin-dependent autophosphorylation
-
-
?
additional information
?
-
-
the enzyme performs Ca2+/calmodulin-dependent autophosphorylation
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-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
CaMKII is a multifunctional enzyme
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
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-
?
additional information
?
-
-
CaMKII performs autophosphorylation, and may also regulate Na+ channels, overview
-
-
?
additional information
?
-
CpkA and CpkC are involved in pathogenicity while CpkB is redundant, CpkA is required for pycnidium development
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-
?
additional information
?
-
no activity with casein, bovine serum albumin, and light chains of various myosins from Dictyostelium, scallop, Mytilis, and chicken
-
-
?
additional information
?
-
-
no activity with casein, bovine serum albumin, and light chains of various myosins from Dictyostelium, scallop, Mytilis, and chicken
-
-
?
additional information
?
-
no activity with casein, bovine serum albumin, and light chains of various myosins from Dictyostelium, scallop, Mytilis, and chicken
-
-
?
additional information
?
-
-
poor or no substrates are kinesin, myosin I, phosvitin, ATP-citrate lyase
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-
?
additional information
?
-
-
cytoskeletal proteins, e.g. vinculin, filamin, fodrin or neurofilament protein
-
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?
additional information
?
-
-
phosphorylase b
-
-
?
additional information
?
-
-
no substrates are protamine
-
-
?
additional information
?
-
-
no substrates are protamine
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?
additional information
?
-
the enzyme is proposed to play a variety of important roles in brain function
-
-
?
additional information
?
-
-
calmodulin-dependent kinase kinase/calmodulin kinase I activity, not CaMKIV or CaMKII, gates extracellular-signal-regulated kinase-dependent long-term potentiation required for learning and memory, Ras-GRF1 and ERK are also involved, NMDA-dependent activation of ERK, CaMKK pathway regulation, overview
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-
?
additional information
?
-
-
CaM kinase II plays a role in diverse cellular processes, the neuronal CaM kinase II is involved in neurotransmitter synthesis and release, modulation of ion cannel activity, cellular transport, cell morphology, regulation of cytoskeleton, and neurite extension, synaptic plasticity, learning and memory, overview, CaM kinase II is involved in memory storage, functional characterization and mechanism, overview, CaMKII is involved in Ca2+-dependent regulation of tyrosine hydroxylase and tryptophan hydroxylase in catecholamin and serotonin biosynthesis, and regulation of monoamine biosynthesis in the brain, CaMKII is involved in PSD in the postsynaptic space, functional analysis including the ion channel activity regulation, e.g. of the NMDA receptor and its NR2B subunit, the glutamate receptor, and the AMPA receptor, and postsynaptic signaling, overview
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-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
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-
?
additional information
?
-
CaMKIgamma is involved in Ca2+ signal transduction in the cytoplasmic compartment of certain neuronal populations
-
-
?
additional information
?
-
-
CaMKII Ca2+/calmodulin-dependently potentiates ATP responses by promoting trafficking of P2X3 receptors, electrical stimulation of dorsal root ganglion neurons or the sciatic nerve enhances the CaMKII-dependent receptor expression in membranes, overview
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?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
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?
additional information
?
-
-
CaMKII is involved in calcium signaling, synaptic plasticity, learning, and memory, CaMKII activity and expression are altered in the hippocampus of Pb2+-exposed rats, reaction velocity is reduced by 41% and substrate affinity is increased by 22%, the rats exhibit deficits in hippocampal log-term potentiation and spatial learning
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?
additional information
?
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CaMKII is reversibly, Ca2+/calmodulin-independently autophosphorylated at Thr286alpha and Thr287beta with inhibitory effect, inactivated and made sedimentable by acute neuronal excitation in rats in vivo, regulation, overview
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?
additional information
?
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-
CASK in inhibited by the plasma membrane Ca2+ pump 4b/CI, PMCA4b, via direct interaction with the C-terminus of the Ca2+ transporter
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?
additional information
?
-
-
glutamate receptor stimulation induces Ca2+-dependent CaMKII translocation to synaptic and nonsynaptic sites
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?
additional information
?
-
-
isozyme CaMKIIdelta3 is involved in the expression of brain-derive neurotrophic factor, BDNF, in the substantia nigra
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?
additional information
?
-
-
the phosphatidylinositol-linked dopamine receptor is involved in regulation of CaMK II enzyme activity in the brain
-
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?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
CaMKII is a multifunctional enzyme
-
-
?
additional information
?
-
-
CaMKII performs autophosphorylation
-
-
?
additional information
?
-
-
CaMKII performs autophosphorylation at Thr286
-
-
?
additional information
?
-
-
isozyme-selective CaMKII binding sequence for interaction with ligand proteins, overview
-
-
?
additional information
?
-
-
CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview
-
-
?
additional information
?
-
-
CaMKII is involved in phorbol ester/ionomycin-induced NFkappaB activation, overview
-
-
?
additional information
?
-
-
CaMKII isozymes have distinct cellular localizations and function, overview, release of acetylcholine from dual transmitting sympathetic neurons requires activation of both the p75 receptor and activated CaMKII, model for neurotrophin-dependent modulation of cholinergic transmission, neurotrophins can influence CaMKII signaling by regulating the production of CaMKII protein and/or by changing the level of CaMKII activation, overview
-
-
?
additional information
?
-
-
CaMKII kinase modulates PC12 cell neuronal differentiation
-
-
?
additional information
?
-
-
CaMKII signaling, overview, CaMKII is essential in the increasing of Ca2+ transient amplitude and production of mechanical contractile recovery from acidosis, two mechanisms, overview
-
-
?
additional information
?
-
-
isozyme CaMKIIdelta regulates cell proliferation of vascular smooth muscle cells, overview
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-
?
additional information
?
-
-
N-methyl-D-aspartate-induced neurotoxicity in the rat retina leads to increased levels of phopshorylated CaMKII and susequently of phosphorylated CREB, overview
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-
?
additional information
?
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-
the enzyme performs autophosphorylation at Thr286 activating the enzyme activity, and at Thr305/Thr306, which inhibits calmodulin binding and enzyme activation
-
-
?
additional information
?
-
-
autophosphorylation is not dependent on calmodulin and Ca2+
-
-
?
additional information
?
-
activated/autophosphorylated CaMKII does not bind to voltage-gated calcium channel subunits beta3 or beta4 subunits
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-
?
additional information
?
-
CaMKIIgamma G2 autophosphorylates in the presence of Ca2+/calmodulin and ATP
-
-
?
additional information
?
-
small C-terminal domain phosphatase-3 dephosphorylates CaMKIIgamma G2, the dephosphorylation is site-specific, excluding the Thr287 associated with Ca2+/calmodulin-independent activation of the kinase, as a result the autonomous activity of CaMKIIgamma G-2 is not affected by the phosphatase activity of small C-terminal domain phosphatase-3
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-
?
additional information
?
-
Thr286-autophosphorylation is antagonistic to CaMKII clustering
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-
?
additional information
?
-
may be important in cell cycle progression
-
-
?
additional information
?
-
-
may be important in cell cycle progression
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
CaMKII is a multifunctional enzyme
-
-
?
additional information
?
-
-
isozyme-selective CaMKII binding sequence for interaction with ligand proteins, overview
-
-
?
additional information
?
-
CaM-KI plays a role in cell structure regulation during early embryonic development
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
isozyme-selective CaMKII binding sequence for interaction with ligand proteins, overview
-
-
?
additional information
?
-
-
calmodulin/CaMKII and ANG II regulate surface expression, recycling, and functional activity of ion channel NBCe1 via separate mechanisms, CaMKII activates NBCe1 expression, overview
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?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + a protein
ADP + a phosphoprotein
ATP + Akt
ADP + phosphorylated Akt
the enzyme (CaMKK2) directly phosphorylates Akt at Thr308
-
-
?
ATP + Blc10
ADP + phosphorylated Blc10
-
Bcl10 is essential for antigen receptor-induced NF-kappaB activation, interleukin-2 production, and T-cell proliferation but is not required for TCR-induced tyrosine phosphorylation, calcium flux, or extracellular signal-regulated kinase activation
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase I
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase I
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation. Ca2+/calmodulin-dependent protein kinase kinase phosphorylates and activates Ca2+/calmodulin-dependent protein kinase I and Ca2+/calmodulin-dependent protein kinase IV, which directly activate transcription factors
-
-
?
ATP + Ca2+/calmodulin-dependent protein kinase IV
ADP + phosphorylated Ca2+/calmodulin-dependent protein kinase IV
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation. Ca2+/calmodulin-dependent protein kinase kinase phosphorylates and activates Ca2+/calmodulin-dependent protein kinase I and Ca2+/calmodulin-dependent protein kinase IV, which directly activate transcription factors
-
-
?
ATP + Cabin1
ADP + phosphorylated Cabin1
-
a transcriptional corepressor of myocyte enhancer factor 2, phosphorylation by CaMKIV creates a docking site for protein 14-3-3, which causes nuclear export, CaMKIV regulates nuclear export of Cabin1 during Ca2+-dependent T-cell activation, regulation overview
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
ATP + cAMP-responsive element-binding protein
ADP + phosphorylated cAMP-responsive element-binding protein
-
i.e. CREB, CaM kinase II, as part of the Ca2+ and CaMK signaling cascade, regulates the phosphorylation of CREB of spinal cord in rats following noxious stimulation, e.g. by capsaicin injection
-
-
?
ATP + CARMA1
ADP + phosphorylated CARMA1
-
CaMKII is a modulator of CARMA1-mediated NF-kappaB activation, overview
-
-
?
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
ATP + CREB1 protein
ADP + phosphorylated CREB1 protein
-
-
-
?
ATP + dystrophin Dp71d
ADP + phosphorylated dystrophin Dp71d
-
the phosphorylation process involves protein kinase C, EC 2.7.11.13, CAMKII-mediated phosphorylation modulates the Dp71 nuclear localization
-
-
?
ATP + Emi2
ADP + phosphorylated Emi2
an APC/C repressor, inactivation
-
-
?
ATP + glutamate receptor subunit GluR1
ADP + phosphorylated glutamate receptor subunit GluR1
-
low activity, CaMKII, membrane localization of GluR1 restricts its phosphorylation
-
-
?
ATP + glutamate receptor subunit NR2B
ADP + phosphorylated glutamate receptor subunit NR2B
-
low activity, CaMKII
-
-
?
ATP + histone deacetylase 4
ADP + phosphorylated histone deacetylase 4
-
the enzyme may facilitate transcription factor activities by the neutralization of histone deacetylase 4 by phosphorylation, which may contribute to the phenotypic plasticity of gastrointestinal smooth muscle cells
-
-
?
ATP + human cardiac sodium channel NaV1.5
ADP + phosphorylated human cardiac sodium channel NaV1.5
-
the intracellular loop between domains 1 and 2 of cardiac sodium channel NaV1.5 is phosphorylated specifically at the Ser516 and Thr594 sites. The phosphorylation status of Ser516 and Thr594 on cardiac sodium channel NaV1.5, is an important mediator of the enzyme-dependent negative shift in cardiac sodium channel NaV1.5
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
ATP + Kir6.2 subunit of cardiac ATP-sensitive potassium channel
ADP + phosphorylated Kir6.2 subunit of cardiac ATP-sensitive potassium channel
-
phosphorylation of Kir6.2 subunit of cardiac ATP-sensitive potassium channel promotes endocytosis of cardiac ATP-sensitive potassium channels
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
ATP + MAP2
ADP + phosphorylated MAP2
-
-
-
-
?
ATP + MEF-2A
ADP + phosphorylated MEF-2A
-
phosphorylation by CaMKIV
-
-
?
ATP + MEF-2C
ADP + phosphorylated MEF-2C
-
phosphorylation by CaMKIV
-
-
?
ATP + MEF-2D
ADP + phosphorylated MEF-2D
-
phosphorylation by CaMKIV
-
-
?
ATP + microtubule affinity regulating kinase 2
ADP + phosphorylated microtubule affinity regulating kinase 2
-
CaMKIalpha/microtubule affinity regulating kinase 2 signaling cascade mediates calcium-dependent neurite outgrowth/axonal extension
-
-
?
ATP + Na+-channel
ADP + phosphorylated Na+-channel
-
isozyme CaMKIIdelta increases persistent/late inward INa and intracellular Na+ concentration regulazing Na+ channel activity, CaMKII expression is increased in heart failure and may be involved in Na+ channel regulation alterations via calmodulin, overview
-
-
?
ATP + NADPH oxidase 5
ADP + phosphoraletd NADPH oxidase 5
-
the enzyme mediates the phosphorylation and activation of NADPH oxidase 5. The ability of Ca2+/calmodulin-dependent protein kinase to regulate NADPH oxidase 5 activity may be significant in the regulation of production of reactive oxygen species that occurs downstream of calcium-mobilizing agonists such as angiotensin II. Of these phosphorylation sites, mutation of only Ser475 to alanine prevents Ca2+/calmodulin-dependent protein kinase-induced increases in activity of NADPH oxidase 5
-
-
?
ATP + neuronal nitric-oxide synthase
ADP + phosphorylated neuronal nitric-oxide synthase
-
phosphorylation at Ser741 by CaM-K Ialpha, wild-type and truncation mutant 1-293 inhibits neuronal nitric-oxide synthase, nNOS, no substrate of CaM-K IIalpha and CaM-K IV
-
-
?
ATP + NFkappaB
ADP + phosphorylated NFkappaB
-
the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536
-
-
?
ATP + NHE-1
ADP + phosphorylated NHE-1
-
phosphorylation by CaMKII is regulated by phosphatase PP1 which is associated with the exchanger
-
-
?
ATP + Notch1 protein
ADP + phosphorylated Notch1 protein
phosphorylation of Notch1 intracellular domain inhibits the proteasomal degradation of Notch1 intracellular domain through Fbw7 ubiquitin-protein ligase complex. Upregulated Notch1 intracellular domain accelerates osteoclast differentiation
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
ATP + PLB
ADP + phosphorylated PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + PLN
ADP + phosphorylated PLN
-
phosphorylation contributes to mechanical recovery from acidosis by inhibiting SERCA2a inhibition
-
-
?
ATP + protein
ADP + phosphorylated protein
ATP + protein CREB
ADP + phosphorylated protein CREB
ATP + protein ERK
ADP + phosphorylated protein ERK
ATP + protein HDAC
ADP + phosphorylated protein HDAC
-
phosphorylation by nuclear CaMKII results in HDAC translocation from nucleus to cytoplasm
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
ATP + protein PLN
ADP + phosphorylated Pprotein LN
-
PLN regulation through phosphorylation by CaMKII at Thr17
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
ATP + PSD-95
ADP + phosphorylated PSD-95
-
high activity, CaMKII, smaller synapses show greater variability in PSD-95 phosphorylation
-
-
?
ATP + Raf-1 protein
ADP + phosphorylated Raf-1 protein
-
the enzyme phosphorylates Raf-1 at Ser338 and mediates Ras-stimulated Raf-1 activation
-
-
?
ATP + ryanodine receptor type 2
ADP + phosphorylated ryanodine receptor type 2
-
i.e. RyR2
-
-
?
ATP + RyR
ADP + phosphorylated RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + S6-kinase
?
-
step of a protein kinase cascade initiated by insulin in a yet unidentified manner
-
-
?
ATP + Stargazin
ADP + phosphorylated Stargazin
-
high activity, CaMKII, phosphatases limit phosphorylation of stargazin
-
-
?
ATP + synapsin
ADP + phosphorylated synapsin
-
-
-
-
?
ATP + synapsin-1
ADP + phopshorylated synapsin-1
-
-
-
-
?
ATP + synGAP
ADP + phosphorylated synGAP
-
regulation and activation of the neuron-specific Ras GTPase-activating protein, synGAP, by phosphorylation through CaMKII in the postsynaptic density fraction of the forebrain, synGAP is part of the signaling complex attached to the cytoplasmic tail of the N-methyl-D-aspartate-type glutamate receptor, overview
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
ATP + vimentin
ADP + phosphorylated vimentin
-
specific phosphorylation by CaMKII at Ser82
-
-
?
additional information
?
-
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
the enzyme phosphorylates e.g. the synaptic vesicle-associated protein synapsin 1 and synapsin 2
-
-
?
ATP + a protein
ADP + a phosphoprotein
-
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
-
-
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
caldesmon plays a role in the regulation of smooth muscle contraction
-
?
ATP + caldesmon
ADP + caldesmon phosphate
-
caldesmon plays a role in the regulation of smooth muscle contraction
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
CaMKIV activates CREB by phosphorylation and stimulates CREB-mediated transcription
-
-
?
ATP + cAMP response element-binding protein
ADP + phosphorylated cAMP response element-binding protein
-
i.e. CREB, phosphorylation by CaMK II at Ser133
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133
-
-
?
ATP + cAMP-response element binding protein
ADP + phosphorylated cAMP-response element binding protein
-
i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142
-
-
?
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
in inner retina, isoform CaMKII-delta colocalizes with connexin36 protein
-
-
?
ATP + connexin36 protein
ADP + phosphorylated connexin36 protein
in the outer and inner retina, isoform CaMKII-beta colocalizes with connexin36-containing gap junctions
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + I-kappaB
ADP + phosphorylated I-kappaB
-
substrate of CaM-KII in T-lymphocytes and neurons, phosphorylation leads to activation of I-kappa B, which mediates activation of NF-kappaB
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-seryl-[protein]
ADP + O-phospho-L-seryl-[protein]
-
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + L-type Ca2+ channel
ADP + phosphorylated L-type Ca2+ channel
-
inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
-
-
?
ATP + phospholamban
ADP + phosphorylated phospholamban
-
phosphorylation by CaMKII activates the sarcoplasmic reticulum Ca2+-ATPase, increasing both the rate of Ca2+ clearance from the myoplasm and the frequency of localized Ca2+ release events from intracellular stores
-
-
?
ATP + protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + protein
ADP + phosphorylated protein
-
-
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
activation by phosphorylation
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
-
the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
activation by phosphorylation
-
-
?
ATP + protein CREB
ADP + phosphorylated protein CREB
-
CaMKII regulates the phosphorylation of CREB in NMDA-induced retinal neurotoxicity
-
-
?
ATP + protein ERK
ADP + phosphorylated protein ERK
activation by phosphorylation
-
-
?
ATP + protein ERK
ADP + phosphorylated protein ERK
activation by phosphorylation
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein PLB
ADP + phosphorylated protein PLB
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + protein RyR
ADP + phosphorylated protein RyR
-
a regulatory protein in Ca2+ signaling
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development, CaM kinase II is involved in the accumulation of tau in neuronal soma in Alzheimer's disease brain
-
-
?
ATP + tau protein
ADP + phosphorylated tau protein
-
phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development
-
-
?
additional information
?
-
involved in neuroplasticity. Mutant caki flies show reduced walking speed in 'Buridan's paradigm'
-
-
?
additional information
?
-
-
CaM kinase II plays a role in diverse cellular processes, overview
-
-
?
additional information
?
-
-
CaMKII is crucial for cellular and behavioral plasticity, autophosphorylation renders the enzyme independent on Ca2+ and calmodulin, which allows it to act as a molecular memory switch, CaMKII is required for memory formation of the brain in specific neurons, Ca2+-independent CaMKII mutant T287D in the adult Drosophila melanogaster CNS enhances plasticity and the training of pheromonal cues, mechanism, overview
-
-
?
additional information
?
-
-
CaM kinase II is strongly phosphorylated by protein kinase A PKA, EC 2.7.11.11, in electrocyte membranes, the activated CaM kinase II 2fold activates the Ca2+ pump and ATPase in the membranes, overview
-
-
?
additional information
?
-
-
protein kinases and protein phosphatases regulate enzyme activities in the cell, overview
-
-
?
additional information
?
-
-
Ca2+ signaling in T-cell activation involves transcriptional activity of MEF-2 and NFAT, which is repressed by Cabin1, activated CaMKIV can overcome the repression by Cabin1, crosstalk between Cabin1 and CaMKIV, dissociation of Cabin1 from MEF-2 by the enzyme requires calmodulin, overview
-
-
?
additional information
?
-
CaM-KI and calcium/calmodulin-dependent kinase kinase CaM-KK participate in the control of cell cycle progression in MCF-7 human breast cancer cells, CaM-KK controls the G0-G1 restriction check point
-
-
?
additional information
?
-
-
CaM-KI and calcium/calmodulin-dependent kinase kinase CaM-KK participate in the control of cell cycle progression in MCF-7 human breast cancer cells, CaM-KK controls the G0-G1 restriction check point
-
-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy, CaMKIIdeltaB expression is increased in heart failure, about 2fold in failing cardiomyopathy, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
components of the Ca2+/calmodulin-dependent protein kinase cascade, overview
-
-
?
additional information
?
-
-
the enzyme is regulated by Ca2+/calmodulin binding and reversible phosphorylation, overview, the autonomous, Ca2+/calmodulin-independent activity of autophosphorylated Ca2+/calmodulin-dependent protein kinase IV is required for its role in transcription
-
-
?
additional information
?
-
-
CaMKII is a major component of the postsynaptic density of excitatory synapses, and plays a key role in the regulation of synaptic function in the mammalian brain, the unique molecular architecture of the postsynaptic density results in highly selective substrate discrimination by CaMKII, overview
-
-
?
additional information
?
-
-
CaMKII substrates CARMA1 and Bcl10 functionally interact and control NF-kappaB signaling downstream of the T-cell receptor
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
-
-
?
additional information
?
-
-
CaMKII regulates P/Q-type Ca2+ current in neurons
-
-
?
additional information
?
-
-
CaMKII binds directly to a site in the C-terminal domain of CaV2.1 channels, autophosphorylation of CaMKII stimulates binding to this site. Autophosphorylated CaMKII can bind to the CaV2.1 channel and synapsin-1 simultaneously. Binding of CaV2.1 to CaMKII induces Ca2+-independent kinase activity, which mediates both autophosphorylation and phosphorylation of synapsin-1 at Ser603. Binding of autophosphorylated CaMKII to GST-tagged CaV2.1(18481964) is substantially greater than binding of nonactivated CaMKII. CaM is not required for CaMKII binding to Ca2+channels. Binding of autophosphorylated CaMKII persists after Ca2+/CaM dissociation
-
-
?
additional information
?
-
-
calmodulin-dependent kinase kinase/calmodulin kinase I activity, not CaMKIV or CaMKII, gates extracellular-signal-regulated kinase-dependent long-term potentiation required for learning and memory, Ras-GRF1 and ERK are also involved, NMDA-dependent activation of ERK, CaMKK pathway regulation, overview
-
-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
CaMKII is required for gene transcription induced in the hippocampus by contextual fear conditioning, alphaCaMKII autophosphorylation is required for memory consolidation-specific transcription and formation of long term potentiation and memory, molecular mechanism, overview
-
-
?
additional information
?
-
-
CaMKIV regulation, overview, CaMKIV functions as a potent stimulator of Ca2+-dependent gene expression
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
-
CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview
-
-
?
additional information
?
-
-
CaMKII is critical in regulating myocyte function with regard to excitation-contraction-relaxation cycles and excitation-transcription coupling
-
-
?
additional information
?
-
-
CaMKII isozymes have distinct cellular localizations and function, overview, release of acetylcholine from dual transmitting sympathetic neurons requires activation of both the p75 receptor and activated CaMKII, model for neurotrophin-dependent modulation of cholinergic transmission, neurotrophins can influence CaMKII signaling by regulating the production of CaMKII protein and/or by changing the level of CaMKII activation, overview
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
-
-
?
additional information
?
-
-
the enzyme is involved in dendritogenesis in cortical neurons and is required for brain-derived neurotropic factor-stimulated dendritic growth, and regulation of dendritic morphogenesis via the lipid-raft-delineated CL3-STEF-RAc pathway contributing to the development of cortical dendrites, overview
-
-
?
additional information
?
-
-
generation of Ca2+-independent activity after Thr286 autophosphorylation is a vital step in regulating synaptic plasticity and learning and memory. The autonomy is substrate-dependent, and low autonomy (15-25%) is the general default
-
-
?
additional information
?
-
in terms of substrate specificity, the consensus sequences for phosphorylation by CaMKI, CaMKII, and CaMKIV are quite similar, and hence these kinases sometimes phosphorylate the same substrates, for example cAMP-response element-binding protein. Expression of Camk2g and Camk2d, but not Camk1 or Camk4, in Camk2g-/- eggs leads to degradation of exogenously expressed EMI2
-
-
?
additional information
?
-
-
in terms of substrate specificity, the consensus sequences for phosphorylation by CaMKI, CaMKII, and CaMKIV are quite similar, and hence these kinases sometimes phosphorylate the same substrates, for example cAMP-response element-binding protein. Expression of Camk2g and Camk2d, but not Camk1 or Camk4, in Camk2g-/- eggs leads to degradation of exogenously expressed EMI2
-
-
?
additional information
?
-
CaMK activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand, RANKL, overview
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
modulating role of CaMK in excitation-contraction coupling in the heart in response to Ca2+ levels, excitation-contraction coupling can be modulated by CaMKII by phosphorylation of several important Ca2+ regulatory proteins in the heart, overview
-
-
?
additional information
?
-
CpkA and CpkC are involved in pathogenicity while CpkB is redundant, CpkA is required for pycnidium development
-
-
?
additional information
?
-
the enzyme is proposed to play a variety of important roles in brain function
-
-
?
additional information
?
-
-
calmodulin-dependent kinase kinase/calmodulin kinase I activity, not CaMKIV or CaMKII, gates extracellular-signal-regulated kinase-dependent long-term potentiation required for learning and memory, Ras-GRF1 and ERK are also involved, NMDA-dependent activation of ERK, CaMKK pathway regulation, overview
-
-
?
additional information
?
-
-
CaM kinase II plays a role in diverse cellular processes, the neuronal CaM kinase II is involved in neurotransmitter synthesis and release, modulation of ion cannel activity, cellular transport, cell morphology, regulation of cytoskeleton, and neurite extension, synaptic plasticity, learning and memory, overview, CaM kinase II is involved in memory storage, functional characterization and mechanism, overview, CaMKII is involved in Ca2+-dependent regulation of tyrosine hydroxylase and tryptophan hydroxylase in catecholamin and serotonin biosynthesis, and regulation of monoamine biosynthesis in the brain, CaMKII is involved in PSD in the postsynaptic space, functional analysis including the ion channel activity regulation, e.g. of the NMDA receptor and its NR2B subunit, the glutamate receptor, and the AMPA receptor, and postsynaptic signaling, overview
-
-
?
additional information
?
-
-
CaM-Ks are involved in cell cycle regulation and centrosome replication, as well as in development of cancer via calmodulin activity, overview, CaM-KI is involved in CDK4/cyclin D1 activity in fibroblasts, CaM-KIV induces CREB-dependent transcription, regulation mechanism, overview, CaM-kinase signaling pathways, it plays a role in anti-apoptotic signaling, overview
-
-
?
additional information
?
-
CaMKIgamma is involved in Ca2+ signal transduction in the cytoplasmic compartment of certain neuronal populations
-
-
?
additional information
?
-
-
CaMKII Ca2+/calmodulin-dependently potentiates ATP responses by promoting trafficking of P2X3 receptors, electrical stimulation of dorsal root ganglion neurons or the sciatic nerve enhances the CaMKII-dependent receptor expression in membranes, overview
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
CaMKII is involved in calcium signaling, synaptic plasticity, learning, and memory, CaMKII activity and expression are altered in the hippocampus of Pb2+-exposed rats, reaction velocity is reduced by 41% and substrate affinity is increased by 22%, the rats exhibit deficits in hippocampal log-term potentiation and spatial learning
-
-
?
additional information
?
-
-
CaMKII is reversibly, Ca2+/calmodulin-independently autophosphorylated at Thr286alpha and Thr287beta with inhibitory effect, inactivated and made sedimentable by acute neuronal excitation in rats in vivo, regulation, overview
-
-
?
additional information
?
-
-
CASK in inhibited by the plasma membrane Ca2+ pump 4b/CI, PMCA4b, via direct interaction with the C-terminus of the Ca2+ transporter
-
-
?
additional information
?
-
-
glutamate receptor stimulation induces Ca2+-dependent CaMKII translocation to synaptic and nonsynaptic sites
-
-
?
additional information
?
-
-
isozyme CaMKIIdelta3 is involved in the expression of brain-derive neurotrophic factor, BDNF, in the substantia nigra
-
-
?
additional information
?
-
-
the phosphatidylinositol-linked dopamine receptor is involved in regulation of CaMK II enzyme activity in the brain
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview
-
-
?
additional information
?
-
-
CaMKII is involved in phorbol ester/ionomycin-induced NFkappaB activation, overview
-
-
?
additional information
?
-
-
CaMKII isozymes have distinct cellular localizations and function, overview, release of acetylcholine from dual transmitting sympathetic neurons requires activation of both the p75 receptor and activated CaMKII, model for neurotrophin-dependent modulation of cholinergic transmission, neurotrophins can influence CaMKII signaling by regulating the production of CaMKII protein and/or by changing the level of CaMKII activation, overview
-
-
?
additional information
?
-
-
CaMKII kinase modulates PC12 cell neuronal differentiation
-
-
?
additional information
?
-
-
CaMKII signaling, overview, CaMKII is essential in the increasing of Ca2+ transient amplitude and production of mechanical contractile recovery from acidosis, two mechanisms, overview
-
-
?
additional information
?
-
-
isozyme CaMKIIdelta regulates cell proliferation of vascular smooth muscle cells, overview
-
-
?
additional information
?
-
-
N-methyl-D-aspartate-induced neurotoxicity in the rat retina leads to increased levels of phopshorylated CaMKII and susequently of phosphorylated CREB, overview
-
-
?
additional information
?
-
-
autophosphorylation is not dependent on calmodulin and Ca2+
-
-
?
additional information
?
-
may be important in cell cycle progression
-
-
?
additional information
?
-
-
may be important in cell cycle progression
-
-
?
additional information
?
-
-
CaMKII is a critical Ca2+ signaling transducer, CaMKII isozyme have special roles in regulating cardiac function determined by their subcellular localization, nuclear CaMKIIdeltaB plays a key role in hypertrophic gene expression, cytosolic CaMKIIdeltaC can affect excitation-contraction-coupling through phosphorylation of Ca2+-regulatory proteins and may introduce signals leading to apoptosis, CaMKII is involved in cardiac hypertrophy and heart failure, signaling pathways, overview, CaMK is involved in regulation of various transcription factors and other DNA-binding proteins, overview
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
CaM-KI plays a role in cell structure regulation during early embryonic development
-
-
?
additional information
?
-
-
Thr286-autophosphorylated CaMKII is associated with CaMKII-binding proteins densin-180, the N-methyl-D-aspartate receptor NR2B subunit, and alpha-actinin-2 in postsynaptic density-enriched rat brain fractions, the proteins influence each other in binding to CaMKII, interaction of binding proteins with CaMKII splicing variants, overview
-
-
?
additional information
?
-
-
calmodulin/CaMKII and ANG II regulate surface expression, recycling, and functional activity of ion channel NBCe1 via separate mechanisms, CaMKII activates NBCe1 expression, overview
-
-
?
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
-
-
2-[4-[6-(quinolin-8-yloxy)pyrimidin-4-yl]piperazin-1-yl]benzonitrile
-
-
-
2-[N-(2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
3-([6-(quinolin-8-yloxy)pyrimidin-4-yl]oxy)aniline
-
-
4-methyl-7-([6-[(quinolin-8-yl)oxy]pyrimidin-4-yl]oxy)-2H-1-benzopyran-2-one
-
6-[(5-methoxy-1H-benzimidazol-2-yl)sulfanyl]-N-(4-methoxyphenyl)pyrimidin-4-amine
-
7-([6-[(5-methoxy-1H-benzimidazol-2-yl)sulfanyl]pyrimidin-4-yl]oxy)-4-methyl-2H-1-benzopyran-2-one
-
7-[(6-chloropyrimidin-4-yl)oxy]-4-methyl-2H-1-benzopyran-2-one
-
7H-benzimidazo(2,1-a)benz(de)isoquinoline-7-one-3-carboxylate
i.e. STO-609. The CaMKKbeta residue Pro274, which replaces the conserved acidic residue of other protein kinases, is an important determinant for the selective inhibition by STO-609. ATP-competitive inhibition mechanism
8-([6-[(5-methoxy-1H-benzimidazol-2-yl)sulfanyl]pyrimidin-4-yl]oxy)quinoline
-
8-([6-[(naphthalen-2-yl)oxy]pyrimidin-4-yl]oxy)-1,4-dihydroquinoline
-
8-[(6-chloropyrimidin-4-yl)oxy]quinoline
-
AC3-I
specific CaMKII inhibitor
AC3-I peptide
-
i.e. autocamtide-2 inhibitory peptide, inhibits CaMKII
ADP
product inhibition is best fit with an Ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus ATP, uncompetitive inhibition versus phospholamban, isoenzyme CaMK IIalpha; product inhibition is best fit with an ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus ATP, uncompetitive inhibition versus phospholamban, isoenzyme CaMK IIbeta; product inhibition is best fit with an Ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus ATP, uncompetitive inhibition versus phospholamban, isoenzyme CaMK IIdelta; product inhibition is best fit with an ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus ATP, uncompetitive inhibition versus phospholamban, isoenzyme CaMK IIgamma
AIP
specific CaMKII inhibitor
ARRKWQKTGHAVRAIGRLSS
-
calmodulin antagonist peptide, IC50: 33.3 nM in H2O, 10.6 nM in buffer containing 0.1% w/v Tween 80
autocamide-2-related inhibitory peptide
-
i.e. AIP, used in its myristoylated form
-
autocamtide 2-related inhibitory peptide
-
-
autocamtide-2 related inhibitory peptide
-
-
-
autocamtide-2-related inhibitory peptide
-
biotinylated Thr-Arg-Ser-Ala-Ile-Arg-Arg-Ala-Ser-Thr-Ile-Glu-Met-Pro-Gln-Gln-Ala-Arg-Gln
product inhibition is best fit with an Ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus phospholamban and ATP, isoenzyme CaMK IIalpha; product inhibition is best fit with an Ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus phospholamban and ATP, isoenzyme CaMK IIbeta; product inhibition is best fit with an Ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus phospholamban and ATP, isoenzyme CaMK IIdelta; product inhibition is best fit with an ordered Bi Bi mechanism in which phospholamban is the first substrate to bind and ADP is the last product to be released. Competitive inhibition versus phospholamban and ATP, isoenzyme CaMK IIgamma
calmodulin antagonist W-7
-
CaM-KIIN
-
noncompetitive inhibitor
-
CaMK phosphatase
specifically dephosphorylates and regulates activity; specifically dephosphorylates and regulates activity; specifically dephosphorylates and regulates activity
-
CaMK-II-Ntide
-
specific CaMK-II inhibitory peptide
-
CaMKI (294-321)
specific CaMKI inhibitor
-
CaMKII (273-302)
specific CaMKII inhibitor
-
CaMKII (281-309)
specific CaMKII inhibitor
-
CaMKIIN
-
brain-specific CaMKII inhibitor
-
CaMKP phosphatase-N
specifically dephosphorylates and regulates activity; specifically dephosphorylates and regulates activity; specifically dephosphorylates and regulates activity
-
CN-21
specific CaMKII inhibitor
curcumin
curcumin strongly interacts with isoform CAMK4
GTP
-
in the presence of ATP
huperzine A
downregulates abnormally high expression of CaMKIIalpha
imatinib
downregulates CaMKIIgamma autophosphorylation/activation
methyl-beta-cyclodextrin
-
-
myristoylated autocamtide-2-related inhibitory peptide
-
-
myristoylated Trp peptide
0.0135 mM prevents alphaCaMKII clustering
N-(4-methoxyphenyl)-6-(piperazin-1-yl)pyrimidin-4-amine
-
-
N-(6-aminohexyl)-1-naphthalenesulfonamide
-
i.e. W7, a calcium-calmodulin inhibitor
NO
a reduction of CaMKII activity by S-nitrosylation at Cys6 is observed, but only after prolonged exposure of over 5 min to NO donors
pea protein peptides
-
purified positively charged peptides produced from pea cellular proteins by alkaline protease, i.e. alcalase, are inhibitory for CaMKII in a competitive manner, especially those with a high content of lysine and arginine, which act more in a mixed inhibition type, amino acid compositions of the peptides and IC50 of peptide fractions, overview
-
PEP-19
specific CaMKII inhibitor
-
Phosphatase 2A
-
not phosphatase 1
-
phosphatidic acid
-
at high concentrations, activates at low concentrations
phosphatidylinositol
-
strong
PMCA4b
-
wild-type PMCA4b inhibits CASK activity, while PMCA4b mutant D672E, containing a point mutation in the ATP binding site, shows only 10% of the wild-type inhibitory potency
-
Protein kinase inhibitor H7
-
weak
-
protein phosphatase 1
negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation
-
Protein phosphatase 2A
negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation
-
protein phosphatase 2B
calcineurin, negative CaMK regulation by dephosphorylation; calcineurin, negative CaMK regulation by dephosphorylation; calcineurin, negative CaMK regulation by dephosphorylation
-
protein phosphatase 2C
negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation
-
protein phosphatase M
negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation; negative CaMK regulation by dephosphorylation
-
quercetin
-
at high concentrations
staurosporine
-
at high concentrations
trifluoperazine dimaleate
W13
-
a calmodulin antagonist
2-[N-(2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
-
KN-93
2-[N-(2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
-
KN93
2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
-
i.e. KN-93
2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)amino-N-(4-chlorocinnamyl)-N-methylbenzylamine
-
i.e. KN-93, competitive on the Ca2+/calmodulin binding site, CaMKII-specific inhibitor, blocks activation of the P2X3 receptor in neurons
AIP peptide
-
a CaMKII inhibitory peptide with the sequence KKALRRQEAVDAL
AIP peptide
-
i.e. autocamtide-2-related inhibitory peptide, comprising 17 amino acids, a CaMKII inhibitory peptide with the sequence KKALRRQEAVDAL
autocamtide-2-related inhibitory peptide
-
specific CaMKII inhibitor
-
autocamtide-2-related inhibitory peptide
-
specific and potent CaMKII inhibitor
-
Ca2+
-
not
Ca2+
-
reversible, kinetics
Calmidazolium
-
calmodulin antagonist
Calmidazolium
-
calmodulin antagonist
Calmidazolium
-
calmodulin antagonist
EGTA
-
-
K252a
-
inhibits CaM-KII
KN-62
-
a Ca2+/calmodulin-dependent enzyme inhibitor
KN-62
specific CaMK inhibitor; specific CaMK inhibitor; specific CaMK inhibitor
KN-62
-
competitive on the Ca2+/calmodulin binding site of CaMKII
KN-93
-
KN-93
-
specific CaM kinase II inhibitor
KN-93
CaM-KI and CaMKII, CaMKI inhibition in vivo causes cell cycle arrest in MCF-7 cells and reduction in cyclin D1 and Rb protein phosphorylation
KN-93
specific CaMK inhibitor; specific CaMK inhibitor; specific CaMK inhibitor
KN-93
inhibits CaMKII activity by blocking its interaction with the Ca2+/calmodulin complex
KN-93
interferes with Ca2+/calmodulin binding; interferes with Ca2+/calmodulin binding
KN-93
-
significant inhibition at 0.01 mM
KN-93
-
selective inhibitor of CaMKII, 5 mg/kg
KN-93
membrane permeant inhibitor of alphaCaMKII binding to Ca2+/calmodulin
KN62
-
inhibits CaMKII
KN62
reversible inhibition, causes inhibition of osteoclast formation in vivo
KN62
-
a CaMKII-specific inhibitor
KN93
-
inhibits CaMKII
KN93
-
binds to the calmodulin-binding site of CaMKII and inhibits its activity
KN93
reversible inhibition, causes inhibition of osteoclast formation in vivo
KN93
-
reversible inhibition of CaMKII
peptide AC3-I
-
i.e. autocamtide-2 inhibitory peptide, inhibits CaMKII
peptide AC3-I
-
i.e. autocamtide-2 inhibitory peptide, inhibits CaMKII
peptide AIP
-
i.e. autocamtide-2-related inhibitory peptide, comprising 17 amino acids, a CaMKII inhibitory peptide with the sequence KKALRRQEAVDAL
peptide AIP
-
i.e. autocamtide-2-related inhibitory peptide, comprising 17 amino acids, a reversible CaMKII inhibitory peptide with the sequence KKALRRQEAVDAL
peptide AIP
-
i.e. autocamtide-2-related inhibitory peptide, comprising 17 amino acids, a CaMKII inhibitory peptide with the sequence KKALRRQEAVDAL
STO-609
the CaM-KKalpha inhibitor STO-609 inhibits activity of the CaM-K1delta truncation mutant 1-296
STO-609
selective inhibitor
trifluoperazine dimaleate
-
calmodulin antagonist
trifluoperazine dimaleate
-
calmodulin antagonist
trifluoperazine dimaleate
-
calmodulin antagonist
W-13
-
calmodulin antagonist
W-13
-
calmodulin antagonist
W-13
-
calmodulin antagonist
W-7
-
a Ca2+/calmodulin antagonist
W-7
-
no inhibition by calcineurin inhibitor FK506
W-7
-
calmodulin antagonist
W-7
-
calmodulin antagonist
W-7
-
calmodulin antagonist
additional information
autoinhibition and activation of the kinase domain of CaMKII. Autoinhibition involves a conformeric equilibrium of the regulatory domain, modulating substrate and nucleotide access. Binding of calmodulin to the regulatory domain induces conformational changes that release the catalytic cleft, activating the kinase and exposing an otherwise inaccessible phosphorylation site, threonine 286. Autophosphorylation at Thr286 further disrupts the interactions between the catalytic and regulatory domains, enhancing the interaction with calmodulin, but maintains the regulatory domain in a dynamic unstructured conformation following dissociation of calmodulin, sustaining activation
-
additional information
-
no inhibition by H-7 and PKI
-
additional information
-
the administration of clonidine, an inhibitor of high-affinity nuclear Ca2+-ATPase, prevents the hypoxia-induced increase in nuclear Ca2+-influx and CaM kinase IV activity
-
additional information
-
synthesis of peptides behaving as autoregulatory pseudosubstrates, determination of inhibitory potential, sequences of autoregulatory regions of the different enzyme forms, required sequence properties, overview
-
additional information
-
CaMKII possesses an autoinhibitory domain, the enzyme is regulated by de-/phosphorylation
-
additional information
-
no inhibition by KN-92, redox regulation of CaM-kinases, inhibition mechanisms, overview
-
additional information
the Ca2+/calmodulin-binding domain overlaps with the autoinhibition domain
-
additional information
-
CaMKIV contains an autoinhibitory domain which harbors the binding site for Ca2+ and calmodulin
-
additional information
-
the enzyme contains an autoinhibitory region close to the active site, which sterically blocks substrate binding
-
additional information
not inhibited by AG490, JAK3 inhibitor, PP1, PD98059, U0126, SB203580, wortmannin, LY294002, c-Jun NH2-terminal kinase inhibitor II, Raf 1 inhibitor, pho kinase inhibitor, RO-31-8220, Go6983, cucurbitacin I, Gleevec, and AMPK inhibitor
-
additional information
calcium-calmodulin dependent signalling via Ca2+ leads to activation of CAMKIV autoinhibition
-
additional information
-
calcium-calmodulin dependent signalling via Ca2+ leads to activation of CAMKIV autoinhibition
-
additional information
-
screening of several compounds containing a pyrimidine scaffold against CAMKIV for inhibitory activity against the enzyme, design and synthesis of several inhibitor compounds containing the pyrimidine scaffold, in vitro fluorescence titration, molecular docking calculations under physiological condition and in silico docking studies, cytotoxicity against human cancer cll lines, overview
-
additional information
-
the enzyme is inhibited by its regulatory subunit masking the active site, autoregulation by a pseudosubstrate mechanism, overview
-
additional information
-
autoinhibitory, in absence of Ca2+/calmodulin the enzyme shows an open conformation with extensive interactions between the C-terminal autoinhibitory sequence and the kinase core influencing the binding site for ATP
-
additional information
-
CaMKII possesses an autinhibitory domain, the enzyme is regulated by de-/phosphorylation
-
additional information
-
no inhibition by KN-92, redox regulation of CaM-kinases, inhibition mechanisms, overview
-
additional information
the Ca2+/calmodulin-binding domain overlaps with the autoinhibition domain
-
additional information
-
the enzyme contains an autoinhibitory region close to the active site, which sterically blocks substrate binding
-
additional information
no inhibition of CaMKII by KN92
-
additional information
-
no inhibition of CaMKII by KN92
-
additional information
-
not inhibited by KN-92
-
additional information
autoinhibition and activation of the kinase domain of CaMKII. Autoinhibition involves a conformeric equilibrium of the regulatory domain, modulating substrate and nucleotide access. Binding of calmodulin to the regulatory domain induces conformational changes that release the catalytic cleft, activating the kinase and exposing an otherwise inaccessible phosphorylation site, threonine 286. Autophosphorylation at Thr286 further disrupts the interactions between the catalytic and regulatory domains, enhancing the interaction with calmodulin, but maintains the regulatory domain in a dynamic unstructured conformation following dissociation of calmodulin, sustaining activation
-
additional information
-
CaMKII possesses an autoinhibitory domain, the enzyme is regulated by de-/phosphorylation
-
additional information
-
the enzyme contains an autoinhibitory region close to the active site, which sterically blocks substrate binding
-
additional information
-
no inhibition by specific inhibitors of protein kinases A or C and Ca2+/calmodulin dependent protein kinase
-
additional information
-
CaMKII is inactivated by autophosphorylation at Thr305 and Thr306
-
additional information
-
CaMKII possesses an autoinhibitory domain, the enzyme is regulated by de-/phosphorylation
-
additional information
-
no inhibition by KN-92, redox regulation of CaM-kinases, inhibition mechanisms, overview
-
additional information
-
R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine, i.e. SCH23390, or the PLCbeta antagonist 1-[6-([17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino)hexyl]-1H-pyrrole-2,5-dione, i.e. U-73122, inhibit CaMK II transactivation by SKF83959 via the brain phosphatidylinositol-linked dopamine receptor, the transactivation is attenuated by calphostin C or by intracellular calcium chelator BAPTA
-
additional information
-
Ca2+ binds to the autoregulatory region of the enzyme disrupting autoinhibitory interactions and allowing access to the catalytic site for substrate and ATP
-
additional information
not affected by myristoyl-RRKEQKTGHAVRAIGRE
-
additional information
-
CaMKII possesses an autoinhibitory domain, the enzyme is regulated by de-/phosphorylation
-
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evolution
calcium/calmodulin-dependent protein kinase IV (CAMKIV) is a member of Ser/Thr protein kinase family
evolution
-
the enzyme belongs to the serine/threonine protein kinase family
malfunction
-
chronic overactivity of CaMKII is associated with left ventricular hypertrophy and dysfunction and lethal arrhythmias
malfunction
deletion causes decreased vascular smooth muscle proliferation, neointimal formation, and programmatic changes in cell cycle control, including increased p21 protein expression and decreased cdk activity
malfunction
-
after CASK silencing, single calcium channel recordings show an increase of the voltage-gated calcium channel Cav1.2 open probability explaining the increase of the whole-cell current
malfunction
autoactivation of CCaMK by mutation of Thr271. The complete absence of the EF-hand domains leads to unregulated Thr271 phosphorylation and deactivation of the protein
malfunction
Camk2b-/- mice, which lack the beta isoform of calcium/calmodulin-dependent protein kinase 2 (CAMK2B), show very severe locomotion deficits, while global deletion of Camk2b in the adult mouse causes only mild locomotion deficits, suggesting that the severe locomotion deficits of Camk2b-/- mice are largely of developmental origin. Early onset deletion of Camk2b in cerebellum, striatum or forebrain do not recapitulate the locomotion deficits, suggesting that these deficits cannot be attributed to a single brain area. Most hippocampal phenotypes observed in Camk2b-/- mutants require CAMK2B protein, but not its enzymatic function
malfunction
CaMKIIalpha inhibition protects from NO-induced neuronal cell death. Isozyme mutation of either site, Cys280 or Cys289, abolishes autonomous Ca2+-independent activity of the isozyme
malfunction
exogenous expression of different cRNAs in isozyme-deficient Camk2gamma-/- eggs shows that the other multifunctional CaM kinases, CaMKI, and CaMKIV, are not capable of substituting CaMKIIgamma to initiate cell cycle resumption in response to a rise in intracellular Ca2+. Exogenous expression of Camk2g or Camk2d results in activation of nearly 80% of Camk2g-/- MII eggs after stimulation with SrCl2. None of the Camk2g-/- MII eggs expressing Camk1 or Camk4 activate in response to SrCl2 treatment. Expression of catalytically inactive CaMKIIgamma mutant K43M in Camk2g-/- eggs to the same level as wild-type Camk2g does not result in EMI2 degradation. Expression of a constitutively active form of Camk4 (ca-Camk4), but not Camk1, triggers egg activation. Female mice lacking CaMKIIgamma are infertile, due to their inability to exit the metaphase II arrest, but they appear morphologically normal
malfunction
loss of either CMK1 or CMK2, or both results in increased expression of cell wall integrity-related genes under Calcofluor white (CFW) treatment. Disruption of either CMK1 or CMK2, or both not only leads to a significant increase of intracellular reactive oxygen species levels, but also leads to a decrease of the mitochondrial membrane potential, suggesting the important roles that CaMKs play in the maintenance of the mitochondrial function. The expression of PGA13, ECM331, DFG5 and CRH11 in cmk2DELTA/DELTA and cmk1DELTA/Dcmk2DELTA/DELTA cells is remarkably upregulated compared with the wild-type strain, while no obvious differences are observed in cmk1DELTA/DELTA cells
malfunction
overexpression and mutation in CAMKIV as well as change in Ca2+ concentration is associated with numerous neurodegenerative diseases and cancers
malfunction
the DELTAcamk-1/DELTAcamk-2, DELTAcamk-4/DELTAcamk-2, and DELTAcamk-3/DELTAcamk-2 double mutants display slow growth phenotype, reduced aerial hyphae, decreased thermotolerance, and increased sensitivity to oxidative stress, revealing the genetic interactions among these kinases
malfunction
the survival of DELTAcamk-2 mutant is increased in induced thermotolerance and oxidative stress conditions. The DELTAcamk-1/DELTAcamk-2, DELTAcamk-4/DELTAcamk-2, and DELTAcamk-3/DELTAcamk-2 double mutants display slow growth phenotype, reduced aerial hyphae, decreased thermotolerance, and increased sensitivity to oxidative stress, revealing the genetic interactions among these kinases
malfunction
-
calcium/calmodulin-dependent protein kinase 2 inhibition or knockdown ameliorates the basic calcium phosphate-induced changes in sry-box 9, indian hedgehog, type X collagen, interleukin-6 and matrix metalloproteinase 13 expression
malfunction
-
enzyme deletion leads to growth defects in different media and increased sensitivity to several environmental stresses, including H2O2, menadione, SDS, and Congo red; they also reduced the ability to produce conidia and traps, thus causing a deficiency in nematicidal ability as well. Moreover, the mutants exhibit hypersensitivity to heat shock and ultraviolet-radiation stresses compared with the wild type strain
malfunction
knockdown or pharmacological inhibition of CaMKK2 produces phenotypes expected of Akt inhibition, including reductions in cell growth and cell viability and in the regulation of Akt downstream targets involved in G1/S transition and apoptosis. CaMKK2 knockdown or inhibition decreases Akt phosphorylation at Thr308 and Ser473
malfunction
the knockdown of isoform CaMKII does not suppress the expression of 20-hydroxyecdysone response genes, such as ECR, USP1, and HR3, in Nilaparvata lugens
malfunction
-
Camk2b-/- mice, which lack the beta isoform of calcium/calmodulin-dependent protein kinase 2 (CAMK2B), show very severe locomotion deficits, while global deletion of Camk2b in the adult mouse causes only mild locomotion deficits, suggesting that the severe locomotion deficits of Camk2b-/- mice are largely of developmental origin. Early onset deletion of Camk2b in cerebellum, striatum or forebrain do not recapitulate the locomotion deficits, suggesting that these deficits cannot be attributed to a single brain area. Most hippocampal phenotypes observed in Camk2b-/- mutants require CAMK2B protein, but not its enzymatic function
-
malfunction
-
loss of either CMK1 or CMK2, or both results in increased expression of cell wall integrity-related genes under Calcofluor white (CFW) treatment. Disruption of either CMK1 or CMK2, or both not only leads to a significant increase of intracellular reactive oxygen species levels, but also leads to a decrease of the mitochondrial membrane potential, suggesting the important roles that CaMKs play in the maintenance of the mitochondrial function. The expression of PGA13, ECM331, DFG5 and CRH11 in cmk2DELTA/DELTA and cmk1DELTA/Dcmk2DELTA/DELTA cells is remarkably upregulated compared with the wild-type strain, while no obvious differences are observed in cmk1DELTA/DELTA cells
-
malfunction
-
the survival of DELTAcamk-2 mutant is increased in induced thermotolerance and oxidative stress conditions. The DELTAcamk-1/DELTAcamk-2, DELTAcamk-4/DELTAcamk-2, and DELTAcamk-3/DELTAcamk-2 double mutants display slow growth phenotype, reduced aerial hyphae, decreased thermotolerance, and increased sensitivity to oxidative stress, revealing the genetic interactions among these kinases
-
malfunction
-
the DELTAcamk-1/DELTAcamk-2, DELTAcamk-4/DELTAcamk-2, and DELTAcamk-3/DELTAcamk-2 double mutants display slow growth phenotype, reduced aerial hyphae, decreased thermotolerance, and increased sensitivity to oxidative stress, revealing the genetic interactions among these kinases
-
malfunction
-
enzyme deletion leads to growth defects in different media and increased sensitivity to several environmental stresses, including H2O2, menadione, SDS, and Congo red; they also reduced the ability to produce conidia and traps, thus causing a deficiency in nematicidal ability as well. Moreover, the mutants exhibit hypersensitivity to heat shock and ultraviolet-radiation stresses compared with the wild type strain
-
metabolism
both signaling by nitric oxide (NO) and by isozyme CaMKIIalpha are implicated in two opposing forms of synaptic plasticity underlying learning and memory, as well as in excitotoxic/ischemic neuronal cell death
metabolism
-
in human hypertrophy, both CaMKII and PKA functionally regulate RyR2 and may induce SR Ca2+ leak. In the transition from hypertrophy to heart failure, the diastolic Ca2+ leak increases and disturbed Ca2+ cycling occurs. This is associated with an increase in CaMKII- but not PKA-dependent RyR2 phosphorylation. PKA-dependent RyR2 phosphorylation is not increased in heart failure and is independent of previous beta-blocker treatment. In heart failure, CaMKII inhibition but not inhibition of PKA yields a reduction of the SR Ca2+ leak. PKA inhibition further reduced SR Ca2+ load and systolic Ca2+ transients. CaMKII inhibition may thus reflect a promising therapeutic target for the treatment of arrhythmias and contractile dysfunction
metabolism
isoform CaMKII-beta is a connexin36-specific regulator in the mouse retina and regulates the primary rod pathway
metabolism
isoform CaMKII-delta is a connexin36-specific regulator in the mouse retina
metabolism
the enzyme cooperatively regulates Ca2+-signaling in Coprinopsis cinerea
metabolism
-
the enzyme cooperatively regulates Ca2+-signaling in Coprinopsis cinerea
-
physiological function
-
Ca2+/calmodulin-dependent protein kinase Ialpha is known as a downstream Ca2+/calmodulin-dependent protein kinase kinase effector, contributes to the aryl hydrocarbon receptor cascade
physiological function
-
CaMKII is capable of regulating the activities of many ion channels and receptors
physiological function
all CaMKII isoenzymes are implicated in a wide variety of cellular processes, which include a critical regulatory role in actin cytoskeletal assembly. All isoforms inhibit polymerization of actin in the order of decreasing effictivenes: CaMKIIbeta, CaMKIIgamma, CaMKIIdelta, CaMKIIalpha. Ca2+/CaM activation of all kinase isoforms produces a robust increase in actin polymerization that surpasses the rates of polymerization in the absence of kinase inhibition
physiological function
all CaMKII isoenzymes are implicated in a wide variety of cellular processes, which include a critical regulatory role in actin cytoskeletal assembly. All isoforms inhibit polymerization of actin in the order of decreasing effictivenes: CaMKIIbeta, CaMKIIgamma, CaMKIIdelta, CaMKIIalpha. Ca2+/CaM activation of all kinase isoforms produces a robust increase in actin polymerization that surpasses the rates of polymerization in the absence of kinase inhibition. The beta isoform bundles actin filaments and sequesters actin monomers in an activity-dependent manner
physiological function
all CaMKII isoenzymes are implicated in a wide variety of cellular processes, which include a critical regulatory role in actin cytoskeletal assembly. All isoforms inhibit polymerization of actin in the order of decreasing effictivenes: CaMKIIbeta, CaMKIIgamma, CaMKIIdelta, CaMKIIalpha. Ca2+/CaM activation of all kinase isoforms produces a robust increase in actin polymerization that surpasses the rates of polymerization in the absence of kinase inhibition. The delta isoform of CaMKII bundles F-actin filaments
physiological function
all CaMKII isoenzymes are implicated in a wide variety of cellular processes, which include a critical regulatory role in actin cytoskeletal assembly. All isoforms inhibit polymerization of actin in the order of decreasing effictivenes: CaMKIIbeta, CaMKIIgamma, CaMKIIdelta, CaMKIIalpha. Ca2+/CaM activation of all kinase isoforms produces a robust increase in actin polymerization that surpasses the rates of polymerization in the absence of kinase inhibition. The gamma isoform induces a layered structure in filaments
physiological function
Ca2+/calmodulin-dependent kinase II controls vascular smooth muscle proliferation through modulation of cell cycle regulators
physiological function
calcium/calmodulin-dependent protein kinase IV enhances osteoclast differentiation via the up-regulation of Notch1 protein stability
physiological function
-
generation of Ca2+-independent activity after Thr286 autophosphorylation is a vital step in regulating synaptic plasticity and learning and memory
physiological function
-
phosphorylation of Kir6.2 subunit of cardiac ATP-sensitive potassium channels promotes endocytosis of cardiac ATP-sensitive potassium channels. This mechanism couples the surface expression of cardiac ATP-sensitive potassium channel with calcium signaling
physiological function
-
the enzyme appears to moderate gastrointestinal smooth muscle cell excitability. Prolonging the activities of Ca2+-sensitive K+ channels in the plasma membrane of gastrointestinal smooth muscle cells is an important regulatory mechanism carried out by the enzyme. It also may facilitate transcription factor activities by the neutralization of histone deacetylase 4 by phosphorylation, which may contribute to the phenotypic plasticity of gastrointestinal smooth muscle cells
physiological function
-
the enzyme can positively regulate NADPH oxidase 5 activity via the phosphorylation of Ser475. The ability of Ca2+/calmodulin-dependent protein kinase to regulate NADPH oxidase 5 activity may be significant in the regulation of production of reactive oxygen species that occurs downstream of calcium-mobilizing agonists such as angiotensin II
physiological function
the enzyme is a member of the CaMK cascade that mediates the response to intracellular Ca2+ elevation
physiological function
-
the enzyme phosphorylates Raf-1 at Ser338 and mediates Ras-stimulated Raf-1 activation
physiological function
the enzyme plays some roles in the embryogenesis in zebrafish
physiological function
-
a complex of CaMKII and CaV2.1 channels is required for short term synaptic plasticity. Calmodulin regulation of Ca2+ channels mediates short term synaptic plasticity and CaMKII bound to CaV2.1 may regulate synaptic plasticity. Binding of CaMKII to CaV2.1 channels induces Ca2+-independent kinase activity
physiological function
camk-1 is essential for growth, circadian clock, and full fertility in Neurospora crassa playing a recessive role in sexual development. The Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
physiological function
camk-2 is essential for full fertility in Neurospora crassa playing a recessive role in sexual development. The Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
physiological function
CAMKII can have both structural and enzymatic functions in the brain. CAMK2B plays an important role in controlling the direction of synaptic plasticity at the parallel fiber. Normal locomotion requires calcium/calmodulin mediated activation of isozyme CAMK2B, but CAMK2B autonomous activity is largely dispensable. Molecular, temporal and region-specific role of CAMK2B in locomotion
physiological function
CaMKIIgamma, the predominant CaMKII isoform in mouse eggs, controls egg activation by regulating cell cycle resumption. Degradation of EMI2 following its phosphorylation specifically by CaMKII is mechanistically linked to and promotes cell cycle resumption in MII eggs
physiological function
enzyme CAMKIV is regulated by the calcium-calmodulin dependent signal through a secondary messenger, Ca2+, which leads to the activation of its autoinhibited form
physiological function
in early Xenopus embryos, CamKII contributes to the establishment of the dorsoventral body axis. During gastrulation, CamKII regulates the separation of mesoderm and ectoderm and is required for convergent extension movements of the dorsal mesoderm. CamKII isoforms interact differentially with the three vertebrate dishevelled proteins, detailed overview. CamKII interacts with dishevelled Dvl2 but not with Dvl1, and Dvl2 is necessary to mediate CamKII function downstream of Dvl1 in convergent extension movements in Xenopus gastrulation. Dvl1 is required for the activation of CamKII and PKC in the wingless/integrated-1 protein (Wnt)/Ca2+ pathway. CamKII preferentially interacts with Dvl2, and Dvl2 strongly interacts with CamKIIdelta and additionally with CamKIIbeta and CamKIIalpha. CamKIIgamma does not interact with any Dvl isoform and Dvl1 does not interact with any of the CamKII isoforms. Interaction between endogenous CamKII and Dvl3 occurs only after Wnt-5a stimulation and at a much lower level than in Dvl2 immunoprecipitates
physiological function
in early Xenopus embryos, CamKII contributes to the establishment of the dorsoventral body axis. During gastrulation, CamKII regulates the separation of mesoderm and ectoderm and is required for convergent extension movements of the dorsal mesoderm. CamKII isoforms interact differentially with the three vertebrate dishevelled proteins, detailed overview. CamKII interacts with dishevelled Dvl2 but not with Dvl1, and Dvl2 is necessary to mediate CamKII function downstream of Dvl1 in convergent extension movements in Xenopus gastrulation. Dvl1 is required for the activation of CamKII and PKC in the wingless/integrated-1 protein (Wnt)/Ca2+ pathway. CamKII preferentially interacts with Dvl2, and Dvl2 strongly interacts with CamKIIdelta and additionally with CamKIIbeta and CamKIIalpha. CamKIIgamma does not interact with any Dvl isoform. and Dvl1 does not interact with any of the CamKII isoforms. Interaction between endogenous CamKII and Dvl3 occurs only after Wnt-5a stimulation and at a much lower level than in Dvl2 immunoprecipitates. The protein complex of Arrb2-Dvl2 and CamKIIdelta regulates convergent extension movements. Enhanced CamKII autophosphorylation in Dvl3-morphant embryos, the convergent extension phenotype in Dvl3-depleted explants is rescued by overexpression of dnCamKIIdelta. In Dvl1/Dvl2 double-morphant embryos, coexpression of CamKIIdelta restores elongation but not constriction of the explants, a phenotype highly reminiscent of the single Dvl2-knockdown phenotype
physiological function
-
In hypertrophy, Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase A (PKA) both phosphorylated RyR2 at levels that were not different from healthy myocardium. In heart failure, the sarcoplasmic reticulum Ca2+ leak is nearly doubled compared with hypertrophy, which leads to reduced systolic Ca2+ transients, a depletion of sarcoplasmic reticulum Ca2+ storage and elevated diastolic Ca2+ levels. This is accompanied by a significantly increased CaMKII-dependent phosphorylation of RyR2. In heart failure, CaMKII inhibition but not inhibition of PKA yields a reduction of the sarcoplasmic reticulum Ca2+ leak
physiological function
isozyme Ca2+/calmodulin-dependent protein kinase IIalpha mediates both long-term potentiation and depression of synaptic strength, as well as excitotoxic neuronal cell death during ischemia, regulation of CaMKII by another second messenger system. For CaMKIIalpha, these functions specifically involve also Ca2+-independent autonomous activity, traditionally generated by Thr286 autophosphorylation. NO-induced S-nitrosylation of CaMKIIalpha also directly generates autonomous activity
physiological function
-
molecular mechanisms of protein kinase regulation by calcium/calmodulin, overview. CASK negatively regulates the cardiac Cav1.2 calcium current expressed in mammalian cell lines via the modulation of the open channel probability. The enzyme interacts and co-localizes with the presynaptic N-type voltage-dependent calcium channel (Cav2.2) in mature hippocampal neurons. CASK has a major role in neurological disorder called X-linked mental retardation
physiological function
the Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
physiological function
the differential calcium binding affinities of the EF-hand domains compared with those of calmodulin suggest that enzyme CCaMK is maintained in the inactive state at basal calcium concentrations and is activated via calmodulin binding during calcium oscillations. Recombinant expression of the kinase domain of CCaMK alone gives rise to spontaneous nodulation 8 weeks after root transformation, but in the absence of rhizobia. The binding of Ca2+ negatively regulates CCaMK by enhancing Thr271 phosphorylation, while binding of calmodulin activates it, the enzyme remains inactive at basal Ca2+ concentrations and becomes activated during Ca2+ spiking. Enzyme regulation modelling, overview
physiological function
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the scaffold protein calcium/calmodulin-dependent serine protein kinase negatively controls ATP release in sensory ganglia upon P2X3 receptor activation and is part of an ATP keeper complex. The ability of P2X3 receptors to transduce extracellular stimuli into neuronal signals critically depends on the dynamic molecular partnership with thecalcium/calmodulin-dependent serine protein kinase, CASK has a negative role in P2X3-mediated ATP release. CASK-controlled ATP efflux follows P2X3 receptor activity, but not depolarization-evoked ATP release. CASK is essential for the transactivation of Panx1 upon P2X3 receptor activation
physiological function
type II Ca2+/calmodulin-dependent protein kinases are involved in the regulation of cell wall integrity and oxidative stress response in Candida albicans. CaMKs are essential for the maintenance of cellular redox balance. CaMKs are important for cell wall integrity under conditions of cell wall stress, and Cmk2 seems to be the main contributor in Candida albicans
physiological function
type II Ca2+/calmodulin-dependent protein kinases are involved in the regulation of cell wall integrity and oxidative stress response in Candida albicans. CaMKs are essential for the maintenance of cellular redox balance. CaMKs are important for cell wall integrity under conditions of cell wall stress, but Cmk1 seems not to be the main contributor in Candida albicans
physiological function
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enzyme activity contributes to basic calcium phosphate crystal-induced changes in chondrocyte phenotypic marker expression
physiological function
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the enzyme (BnaCPK2) plays an important role in reactive oxygen species and cell death control through interacting with respiratory burst oxidase homolog D (RbohD)
physiological function
the enzyme (CaMKK2) regulates the growth and viability of OVCa cells
physiological function
the enzyme is associated with cerebral hypoxia, cancer, and neurodegenerative diseases
physiological function
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the enzyme is involved in regulating multiple cellular processes, such as growth, environmental stress tolerance, conidiation, trap formation, and virulence of Arthrobotrys oligospora
physiological function
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the scaffold protein calcium/calmodulin-dependent serine protein kinase negatively controls ATP release in sensory ganglia upon P2X3 receptor activation and is part of an ATP keeper complex. The ability of P2X3 receptors to transduce extracellular stimuli into neuronal signals critically depends on the dynamic molecular partnership with thecalcium/calmodulin-dependent serine protein kinase, CASK has a negative role in P2X3-mediated ATP release. CASK-controlled ATP efflux follows P2X3 receptor activity, but not depolarization-evoked ATP release. CASK is essential for the transactivation of Panx1 upon P2X3 receptor activation
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physiological function
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CAMKII can have both structural and enzymatic functions in the brain. CAMK2B plays an important role in controlling the direction of synaptic plasticity at the parallel fiber. Normal locomotion requires calcium/calmodulin mediated activation of isozyme CAMK2B, but CAMK2B autonomous activity is largely dispensable. Molecular, temporal and region-specific role of CAMK2B in locomotion
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physiological function
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type II Ca2+/calmodulin-dependent protein kinases are involved in the regulation of cell wall integrity and oxidative stress response in Candida albicans. CaMKs are essential for the maintenance of cellular redox balance. CaMKs are important for cell wall integrity under conditions of cell wall stress, and Cmk2 seems to be the main contributor in Candida albicans
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physiological function
-
type II Ca2+/calmodulin-dependent protein kinases are involved in the regulation of cell wall integrity and oxidative stress response in Candida albicans. CaMKs are essential for the maintenance of cellular redox balance. CaMKs are important for cell wall integrity under conditions of cell wall stress, but Cmk1 seems not to be the main contributor in Candida albicans
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physiological function
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camk-2 is essential for full fertility in Neurospora crassa playing a recessive role in sexual development. The Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
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physiological function
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the Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
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physiological function
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camk-1 is essential for growth, circadian clock, and full fertility in Neurospora crassa playing a recessive role in sexual development. The Ca2+/CaMK isozymes are involved in growth, thermotolerance, oxidative stress tolerance, and fertility in Neurospora crassa
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physiological function
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the enzyme is involved in regulating multiple cellular processes, such as growth, environmental stress tolerance, conidiation, trap formation, and virulence of Arthrobotrys oligospora
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additional information
CAMKIV structure-function analysis, pH dependence, molecular dynamics simulations and three-dimensional structure analysis, overview
additional information
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CAMKIV structure-function analysis, pH dependence, molecular dynamics simulations and three-dimensional structure analysis, overview
additional information
modelling of two stable states for CCaMK: an inactive form that predominates at basal Ca2+ concentrations and involves a hydrogen bond network between the CaM binding and kinase domains and an active form that predominates during Ca2+ oscillations associated with CaM binding. The hydrogen bond between phosphorylated Thr271 and Ser322 is the predominant stabilizing bond at the inactive fold in Medicago truncatula CCaMK
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T286E/D135N
phosphomimic mutant, lower melting temperature. Distinct changes in backbone order upon binding of Ca2+/CaM to the T286E/D135N mutant
T287D
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site-directed mutagenesis, the Ca2+-independent mutant expression leads to reduced viability of flies, the toxic effect can be rescued by tetracycline, expression of the mutant in brain mushroom bodies does not affect the immediate memory, overview
K60E
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mutant is kinase dead
E60G
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the mutation exerts different effects on the kinetic parameters of phosphorylation of GluN2B and GluN2A, of which only GluN2B binds to the T-site of the enzyme. GluN2B-induced modulation of the kinetic parameters of peptide substrate is altered in the mutant. The mutation almost abolishes the modulation of the apparent Km value for protein substrate. When GST-tagged GluN2A is used as the substrate, the rate of phosphorylation of the mutant decreases considerably as seen by a 4.3fold reduction in kcat in comparison with that of wild type enzyme. The mutant does not exhibit calcium-independent activity
F320D/N321D
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site-directed mutagenesis, the mutation changes the sequence FNDD to DDDD, the mutant shows no binding of calmodulin and increased activity in nonphosphorylated status compared to the wild-type enzyme
I205K
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site-directed mutagenesis, the mutant CaMKII shows reduced activity with vimentin compared to the wild-type enzyme
K75E
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site-directed mutagenesis, catalytically inactive CaMKIV mutant
P274E
the P274E mutation significantly reduces the inhibitory effect of 7H-benzimidazo(2,1-a)benz(de)isoquinoline-7-one-3-carboxylate (i.e. STO-609) on the isoenzyme CaMKKbeta
T180A
site-directed mutagenesis, the mutant enzyme shows highly reduced activity compared to the wild-type enzyme, the mutant is phosphorylated and activated by CaM-KKalpha
T200A
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site-directed mutagenesis, the mutant CaMKIV is not phosphorylated by CaMKKbeta and is thus incapable of developing autonomous activity and control gene transcription, the same effect occurs due to combination of T200A with calmodulin binding site mutations, overview
T287D
constitutively active CaMKIId mutant
T287D/K43M
kinase dead CaMKIId mutant
alpha11beta
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-11 isoform alpha, exon 12-20 isoform beta, affinity for calmodulin, type low
alpha2beta
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-2 isoform alpha, exon 3-20 isoform beta, affinity for calmodulin, type middle
alpha9beta
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-9 isoform alpha, exon 10-20 isoform beta, affinity for calmodulin, type middle
beta11alpha
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-11 isoform beta, exon 12-17 isoform alpha, affinity for calmodulin, high
beta2alpha
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-2 isoform beta, exon 3-17 isoform alpha, affinity for calmodulin, type lower than low
beta9alpha |
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chimera Ca2+/calmodulin-dependent protein kinase II, exon 1-9 isoform beta, exon 10-17 isoform alpha, affinity for calmodulin, type lower than low
E319A
site-directed mutagenesis, Thr271 phosphorylation is reduced in the mutant compared to the wild-type
L324A
site-directed mutagenesis, Thr271 phosphorylation is abolished in the L324A mutant compared to the wild-type
L333A
site-directed mutagenesis, Thr271 phosphorylation is enhanced in the L324A mutant compared to the wild-type, resulting in a constitutively active enzyme
R323A
site-directed mutagenesis, the mutant is unable to autoactivate
S322A
site-directed mutagenesis, the mutant is able to autoactivate
S343A
site-directed mutagenesis, Thr271 phosphorylation is reduced in the mutant compared to the wild-type
T271A
site-directed mutagenesis, the mutant is able to autoactivate
T271D
site-directed mutagenesis, the mutant is able to autoactivate
T271I
site-directed mutagenesis, the mutant is able to autoactivate
T271X
autoactivation of CCaMK by mutation of Thr271
A303R
site-directed mutagenesis, the mutation interferes with calcium/calmodulin binding and activation of CAMK2B, as well as the autonomous (calcium/calmodulin-independent) activity of CAMK2B, and renders CAMK2B into a persistently F-actin bound state
C417S/C419S/C420S/C423S
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site-directed mutagenesis, mutation of palmitoylation sites
K42M/T286D
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inactive CaMKII mutant
K43M
site-directed mutagenesis, catalytically inactive form of CaMKIIgamma
K52A
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site-directed mutagenesis, inactive mutant, loss-of-function in embryonic cortical neurons elicits a specific impairment in dendrite morphogenesis
T200A
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site-directed mutagenesis, phosphorylation site mutant of CaMKIV, no activation by phosphorylation through CaMKK, no stimulation by ionomycin in absence of Ca2+ and calmodulin
T286A
mutant shows 50% reduction in phosphorylation activity
T286D
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constitutively active CaMKII mutant
T287A
site-directed mutagenesis, an autophosphorylation-deficient CAMK2B mouse mutant. Nearly complete absence of T287-phosphorylated CAMK2B in Camk2bT287A/T287A mice without changes in T286-phosphorylated CAMK2A or total levels of both CAMK2A and CAMK2B
A303R
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site-directed mutagenesis, the mutation interferes with calcium/calmodulin binding and activation of CAMK2B, as well as the autonomous (calcium/calmodulin-independent) activity of CAMK2B, and renders CAMK2B into a persistently F-actin bound state
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T287A
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site-directed mutagenesis, an autophosphorylation-deficient CAMK2B mouse mutant. Nearly complete absence of T287-phosphorylated CAMK2B in Camk2bT287A/T287A mice without changes in T286-phosphorylated CAMK2A or total levels of both CAMK2A and CAMK2B
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L916R
site-directed mutagenesis, mutation in the calmodulin binding site residue abolishes the calmodulin binding
R924E/K925E/K926E/K927E
site-directed mutagenesis, mutations break the basic amphiphilic alpha-helix structure of the calmodulin binding site, the mutant is not capable of calmodulin binding
W919R
site-directed mutagenesis, mutation in the calmodulin binding site residue abolishes the calmodulin binding
A302R
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mutation impairs Ca2+/calmodulin-binding
I205K
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site-directed mutagenesis, the mutant CaMKII does not undergo self-association in recombinant HEK-293 cells
K42M/T286D
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inactive CaMKII mutant
K42R
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mutation without enzymatic activity
K52E
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site-directed mutagenesis, inactive mutant
K52E/I286E/H287D/Q288D/S289D/W303S/F307A
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site-directed mutagenesis of CaMKIalpha isozyme, the mutant is inactive and unable to bind Ca2+ and calmodulin
T287D
constitutively active mutant
K50E
site-directed mutagenesis and truncation mutation constructing mutant K50E 1-295, the mutant isozyme CaM-KIalpha is constitutively active
K53E
site-directed mutagenesis and truncation mutation constructing mutant K50E 1-297, the mutant isozyme CaM-KI LiKbeta is constitutively active
T286A
site-directed mutagenesis
T286A
mutant clustering behaviour is similar compared to the wild type enzyme
T286A
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the mutant is constitutively active and capable of only transient Ca2+-dependent activation
T286D
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site-directed mutagenesis, the mutant CaMKII exhibits poor self-association in recombinant HEK-293 cells and is impaired in autophosphorylation
T286D
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site-sirected mutagenesis of alpha isozyme residue, the mutant is impaired in autophosphorylation and completely in neurite extension
T286D
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site-sirected mutagenesis of alpha isozyme residue, the mutant is impaired in autophosphorylation and partially in neurite extension
T286D
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constitutively active CaMKII mutant
T286D
mutant mimics autophosphorylation at Thr286
T286D
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the mutant is constitutively active and Ca2+-independent
additional information
construction the cmk1DELTA/DELTA, the cmk2DELTA/DELTA and the cmk1DELTA/DELTA-cmk2DELTA/DELTA deletion mutants. CaMK mutants show no growth defect
additional information
construction the cmk1DELTA/DELTA, the cmk2DELTA/DELTA and the cmk1DELTA/DELTA-cmk2DELTA/DELTA deletion mutants. CaMK mutants show no growth defect
additional information
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construction the cmk1DELTA/DELTA, the cmk2DELTA/DELTA and the cmk1DELTA/DELTA-cmk2DELTA/DELTA deletion mutants. CaMK mutants show no growth defect
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additional information
CaMKI 1-306, is unable to bind Ca2+-calmodulin and is completely inactive. CaMKI 1-294 does not bind CaM but is fully active in the absence of Ca2+-calmodulin. CaMKI is phosphorylated on Thr177 and its activity enhances approximately 25-fold by CaMKI kinase in a Ca2+-calmodulin dependent manner. CaMKI 1-306 is unresponsive to CaMKI kinase, the 1-294 mutant is phosphorylated and activated by CaMKI kinase in both the presence and absence of Ca(2+)-CaM although at a faster rate in its presence. Replacement of Thr177 with Ala or Asp prevented both phosphorylation and activation by CaMKI kinase and the latter replacement also leads to partial activation in the absence of CaMKI kinase
additional information
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CaMKI 1-306, is unable to bind Ca2+-calmodulin and is completely inactive. CaMKI 1-294 does not bind CaM but is fully active in the absence of Ca2+-calmodulin. CaMKI is phosphorylated on Thr177 and its activity enhances approximately 25-fold by CaMKI kinase in a Ca2+-calmodulin dependent manner. CaMKI 1-306 is unresponsive to CaMKI kinase, the 1-294 mutant is phosphorylated and activated by CaMKI kinase in both the presence and absence of Ca(2+)-CaM although at a faster rate in its presence. Replacement of Thr177 with Ala or Asp prevented both phosphorylation and activation by CaMKI kinase and the latter replacement also leads to partial activation in the absence of CaMKI kinase
additional information
CaM-K1delta 1-296 truncation mutant is catalytically active and Ca2+/calmodulin-independent, lacks the putative autoinhibitory domain and the Ca2+/calmodulin binding region, the truncation mutant is fully activated by CaM-KKalpha
additional information
CaM-KI inhibition by expression of siRNA causes cell cycle arrest in MCF-7 cells
additional information
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CaM-KI inhibition by expression of siRNA causes cell cycle arrest in MCF-7 cells
additional information
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introduction of lentivirus shRNA specific for human CaMKIV into human T-cells and Jurkat cells leads to knockdown of CaMKIV expression
additional information
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mutation of residues N300, N306, N312, N318, N324, N330, N336, N341, and N347 for determination of residues involved in calmodulin binding, no binding of calmodulin and increased activity compared to the wild-type enzyme by nonphosphorylated mutants of N318, N324, N330, and N336, overview
additional information
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siRNa silencing of CASK after its transfection in TsA-201 cells. The CASK silencing does not modulate Cav1.2 subunits expression, the effect mediated by CASK silencing is a dynamic process. Silencing of CASK increase the open probability of the calcium channel via activation of calcineurin through cleavage by a phosphatase
additional information
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construction of transgenic mice overexpressing calmodulin, the mutant mice develop severe cardiac hypertrophy and show increased Ca2+/calmodulin-independent CaMKII activity, overexpression of CaMKIV and CaMKIV knockout also lead to development of cardiac hypertrophy, CaMKIIdeltaB overexpressing transgenic mice do not phosphorylate CREB
additional information
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deficiency in autophosphorylation in mice leads to impaired upregulation of an associative transcript, the nerve growth factor-inducible gene B messenger RNA, overview
additional information
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construction of transgenic mice expressing the AIP inhibitory peptide in cardiomyocytes nuclei, the inhibitor affects the nuclear enzyme, but not the cytoplasmic enzyme, which inhibits the translocation of protein HDAC5 from nucleus to cytoplasm, phenotype, overview
additional information
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transgenic CaMKIIdelta overexpression prolongs QRS duration and repolarization, i.e. QT intervals, decreases effective refractory periods, and increases the propensity to develop ventricular tachyarrhythmia, overview, CaMKIIdelta enhances steady-state inactivation of transgenic rabbit myocyte sodium current INa, steady-state inactivation, overview
additional information
generation of a Camk2b knockout mutants by deletion of exon 11
additional information
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generation of a Camk2b knockout mutants by deletion of exon 11
additional information
generation of isozyme-deficient Camk2gamma-/- eggs, exogenous expression of different cRNAs in the mutant eggs shows that the other multifunctional CaM kinases, CaMKI, and CaMKIV, are not capable of substituting CaMKIIgamma to initiate cell cycle resumption in response to a rise in intracellular Ca2+. Exogenous expression of Camk2g or Camk2d results in activation of nearly 80% of Camk2g-/- MII eggs after stimulation with SrCl2. None of the Camk2g-/- MII eggs expressing Camk1 or Camk4 activate in response to SrCl2 treatment. Expression of a constitutively active form of Camk4 (ca-Camk4), but not Camk1, triggers egg activation
additional information
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generation of isozyme-deficient Camk2gamma-/- eggs, exogenous expression of different cRNAs in the mutant eggs shows that the other multifunctional CaM kinases, CaMKI, and CaMKIV, are not capable of substituting CaMKIIgamma to initiate cell cycle resumption in response to a rise in intracellular Ca2+. Exogenous expression of Camk2g or Camk2d results in activation of nearly 80% of Camk2g-/- MII eggs after stimulation with SrCl2. None of the Camk2g-/- MII eggs expressing Camk1 or Camk4 activate in response to SrCl2 treatment. Expression of a constitutively active form of Camk4 (ca-Camk4), but not Camk1, triggers egg activation
additional information
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generation of a Camk2b knockout mutants by deletion of exon 11
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additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
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generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
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generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
additional information
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generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview. Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
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additional information
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generation of diverse single and double deletion mutants of genes camk-1-camk-4, phenotypes with reduced thermotolerance and increased sensitivity to oxidative stress, complementation studies with other camk genes, overview, Mutant DELTAcamk-2 shows increased thermotolerance, while all other camk mutants show decreased thermotolerance
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additional information
disruptions of genes CpkA, CpkB, and CpkC do not affect fungal growth or pathogenicity, but CpkC deficiency leads to delayed lesion development and sporulation during infection, mycelia deficient in CpkA show a phenotype with mycelia lighter in colour, highly reduced sporulation activity, and reduced asexually formed pycnidia, overview
additional information
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CaMKII downregulation by CaMKII small interfering RNA in retinal cells
additional information
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overexpression of CaMKII favors the Dp71d nuclear accumulation
additional information
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CaMKII1-290 is a truncated sequence of CaMKII that makes the enzyme constitutively active
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