2.7.11.17 ATP + a protein - 2.7.11.17 ATP + a protein the enzyme phosphorylates e.g. the synaptic vesicle-associated protein synapsin 1 and synapsin 2 2.7.11.17 ATP + Akt the enzyme (CaMKK2) directly phosphorylates Akt at Thr308 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + caldesmon - 2.7.11.17 ATP + caldesmon caldesmon plays a role in the regulation of smooth muscle contraction 2.7.11.17 ATP + cAMP response element-binding protein CaMKIV activates CREB by phosphorylation and stimulates CREB-mediated transcription 2.7.11.17 ATP + cAMP response element-binding protein i.e. CREB, phosphorylation by CaMK II at Ser133 2.7.11.17 ATP + cAMP-response element binding protein i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133 2.7.11.17 ATP + cAMP-response element binding protein i.e. CREB, phosphorylation by CaMKII and CaMKIV at Ser133, and phosphorylation by CaMKII at Ser142 2.7.11.17 ATP + 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 2.7.11.17 ATP + CARMA1 CaMKII is a modulator of CARMA1-mediated NF-kappaB activation, overview 2.7.11.17 ATP + connexin36 protein in inner retina, isoform CaMKII-delta colocalizes with connexin36 protein 2.7.11.17 ATP + connexin36 protein in the outer and inner retina, isoform CaMKII-beta colocalizes with connexin36-containing gap junctions 2.7.11.17 ATP + CREB1 protein - 2.7.11.17 ATP + dystrophin Dp71d the phosphorylation process involves protein kinase C, EC 2.7.11.13, CAMKII-mediated phosphorylation modulates the Dp71 nuclear localization 2.7.11.17 ATP + Emi2 an APC/C repressor, inactivation 2.7.11.17 ATP + glutamate receptor subunit GluR1 low activity, CaMKII, membrane localization of GluR1 restricts its phosphorylation 2.7.11.17 ATP + glutamate receptor subunit NR2B low activity, CaMKII 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + L-seryl-[protein] - 2.7.11.17 ATP + L-type Ca2+ channel inactivation, leading to increased Ca2+ channel open probability and increased arrhytmias 2.7.11.17 ATP + MAP2 - 2.7.11.17 ATP + MEF-2A phosphorylation by CaMKIV 2.7.11.17 ATP + MEF-2C phosphorylation by CaMKIV 2.7.11.17 ATP + MEF-2D phosphorylation by CaMKIV 2.7.11.17 ATP + microtubule affinity regulating kinase 2 CaMKIalpha/microtubule affinity regulating kinase 2 signaling cascade mediates calcium-dependent neurite outgrowth/axonal extension 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + 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 2.7.11.17 ATP + NFkappaB the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536 2.7.11.17 ATP + NHE-1 phosphorylation by CaMKII is regulated by phosphatase PP1 which is associated with the exchanger 2.7.11.17 ATP + 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 2.7.11.17 ATP + phospholamban - 2.7.11.17 ATP + 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 2.7.11.17 ATP + PLB a regulatory protein in Ca2+ signaling 2.7.11.17 ATP + PLN phosphorylation contributes to mechanical recovery from acidosis by inhibiting SERCA2a inhibition 2.7.11.17 ATP + protein - 2.7.11.17 ATP + protein CREB activation by phosphorylation 2.7.11.17 ATP + protein CREB CaMKII regulates the phosphorylation of CREB in NMDA-induced retinal neurotoxicity 2.7.11.17 ATP + protein CREB the nuclear CaMKII does not phosphorylate, in contrast to the cytoplasmic isozyme, CREB at S133 and NFkappaB at S536 2.7.11.17 ATP + protein ERK activation by phosphorylation 2.7.11.17 ATP + protein HDAC phosphorylation by nuclear CaMKII results in HDAC translocation from nucleus to cytoplasm 2.7.11.17 ATP + protein PLB a regulatory protein in Ca2+ signaling 2.7.11.17 ATP + protein PLN PLN regulation through phosphorylation by CaMKII at Thr17 2.7.11.17 ATP + protein RyR a regulatory protein in Ca2+ signaling 2.7.11.17 ATP + PSD-95 high activity, CaMKII, smaller synapses show greater variability in PSD-95 phosphorylation 2.7.11.17 ATP + Raf-1 protein the enzyme phosphorylates Raf-1 at Ser338 and mediates Ras-stimulated Raf-1 activation 2.7.11.17 ATP + ryanodine receptor type 2 i.e. RyR2 2.7.11.17 ATP + RyR a regulatory protein in Ca2+ signaling 2.7.11.17 ATP + S6-kinase step of a protein kinase cascade initiated by insulin in a yet unidentified manner 2.7.11.17 ATP + Stargazin high activity, CaMKII, phosphatases limit phosphorylation of stargazin 2.7.11.17 ATP + synapsin - 2.7.11.17 ATP + synapsin-1 - 2.7.11.17 ATP + 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 2.7.11.17 ATP + tau protein phosphorylation at Ser416 by CaM kinase II is high in early stages of brain development 2.7.11.17 ATP + 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 2.7.11.17 ATP + vimentin specific phosphorylation by CaMKII at Ser82 2.7.11.17 additional information involved in neuroplasticity. Mutant caki flies show reduced walking speed in 'Buridan's paradigm' 2.7.11.17 additional information may be important in cell cycle progression 2.7.11.17 additional information the enzyme is proposed to play a variety of important roles in brain function 2.7.11.17 additional information protein kinases and protein phosphatases regulate enzyme activities in the cell, overview 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 additional information CaM kinase II plays a role in diverse cellular processes, overview 2.7.11.17 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 2.7.11.17 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 2.7.11.17 additional information CaM-KI plays a role in cell structure regulation during early embryonic development 2.7.11.17 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 2.7.11.17 additional information CaMKIgamma is involved in Ca2+ signal transduction in the cytoplasmic compartment of certain neuronal populations 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 additional information CaMKIV regulation, overview, CaMKIV functions as a potent stimulator of Ca2+-dependent gene expression 2.7.11.17 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 2.7.11.17 additional information components of the Ca2+/calmodulin-dependent protein kinase cascade, overview 2.7.11.17 additional information glutamate receptor stimulation induces Ca2+-dependent CaMKII translocation to synaptic and nonsynaptic sites 2.7.11.17 additional information isozyme CaMKIIdelta3 is involved in the expression of brain-derive neurotrophic factor, BDNF, in the substantia nigra 2.7.11.17 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 2.7.11.17 additional information the phosphatidylinositol-linked dopamine receptor is involved in regulation of CaMK II enzyme activity in the brain 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 additional information CaMKI isozymes play distinct roles in hippocampal dendritic growth and neuronal development, overview 2.7.11.17 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 2.7.11.17 additional information CaMKII is critical in regulating myocyte function with regard to excitation-contraction-relaxation cycles and excitation-transcription coupling 2.7.11.17 additional information CaMKII is involved in phorbol ester/ionomycin-induced NFkappaB activation, overview 2.7.11.17 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 2.7.11.17 additional information CaMKII kinase modulates PC12 cell neuronal differentiation 2.7.11.17 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 2.7.11.17 additional information CaMKII substrates CARMA1 and Bcl10 functionally interact and control NF-kappaB signaling downstream of the T-cell receptor 2.7.11.17 additional information CpkA and CpkC are involved in pathogenicity while CpkB is redundant, CpkA is required for pycnidium development 2.7.11.17 additional information isozyme CaMKIIdelta regulates cell proliferation of vascular smooth muscle cells, overview 2.7.11.17 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 2.7.11.17 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 2.7.11.17 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 2.7.11.17 additional information autophosphorylation is not dependent on calmodulin and Ca2+ 2.7.11.17 additional information CaMKII regulates P/Q-type Ca2+ current in neurons 2.7.11.17 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 2.7.11.17 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(1848–1964) 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 2.7.11.17 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