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The data suggest T287 autophosphorylation regulates substrate gating, an intrinsic property of the catalytic domain, which is amplified within the multivalent architecture of the calcium/calmodulin-dependent protein kinase II holoenzyme.
These findings indicate that the CaMKII-mediated GluA1 (show GRIA1 Proteins) phosphorylation of S567 and S831 is critical for P2X2 (show P2RX2 Proteins)-mediated AMPAR internalization and ATP-driven synaptic depression.
Laminin is instructive and CaMKII is non-permissive for the formation of complex aggregates of acetylcholine receptors on myotubes in culture.
A new molecular mechanism mediated by CAMK2gamma in intestinal epithelial cells during colitis-associated cancer (CAC (show CA2 Proteins)) development, thereby providing a potential new therapeutic target for CAC (show CA2 Proteins).
oxidative stress activated the TRPM2 (show CLU Proteins)-CaMKII cascade to further induce intracellular ROS (show ROS1 Proteins) production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
CKIalpha (show CSNK1A1 Proteins)-mediated NS5A S235 phosphorylation is critical for HCV replication. CaMKII gamma and delta may have negative roles in the HCV life cycle.
Demonstrate that calcium/CaMKIIgamma/AKT (show AKT1 Proteins) signaling can regulate apoptosis and autophagy simultaneously in colorectal cancer cells.
Dysfunction in CaMKII-based signaling has been linked with a host of cardiovascular phenotypes including heart failure and arrhythmia, and CaMKII levels are elevated in human and animal disease models of heart disease.
Inhibition of CaMKII activity results in an upregulation of CaMKIV (show CAMK4 Proteins) mRNA and protein in leukemia cell lines.
CAMKIIgamma, HSP70 (show HSP70 Proteins) and HSP90 (show HSP90 Proteins) transcripts are differentially expressed in chronic myeloid leukemia (show BCL11A Proteins) cells from patients with resistant mutated disease.
Redox-sensitive activation of p38 MAPK (show MAPK14 Proteins)/HSP27 (show HSPB1 Proteins) pathway or ERK1/2 in endothelial cells requires CaMKII
Data, including data from studies using transgenic mice, suggest that signaling via prostaglandin-F2alpha/PTGFR (show PTGFR Proteins) and Camk2g/p38 (show CRK Proteins)/Foxo1 (show FOXO1 Proteins) MAP kinase (show MAPK1 Proteins)/calcium pathways are involved in regulation of hepatic gluconeogenesis in both obesity and fasting. (Ptgfr (show PTGFR Proteins) = prostaglandin F2alpha receptor (show PTGFR Proteins); Camk2g = calcium-calmodulin-dependent protein kinase type 2 gamma; p38 (show CRK Proteins) = p38 MAP kinase (show MAPK14 Proteins); Foxo1 (show FOXO1 Proteins) = forkhead box transcription factor (show FOXP2 Proteins) O1)
RGS6 (show RGS6 Proteins) and oxidized CaMKIIdelta together function as novel critical upstream modulators of Notch (show NOTCH1 Proteins) signaling required for normal cardiovascular development and embryo survival.
CaMKIIgamma-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIgamma had increased expression of the transcription factor ATF6 (show ATF6 Proteins).
A new molecular mechanism mediated by CAMK2gamma in intestinal epithelial cells during colitis-associated cancer (CAC (show SLC25A20 Proteins)) development, thereby providing a potential new therapeutic target for CAC (show SLC25A20 Proteins).
Data indicate that combined cardiomyocyte-specific deletion of CaM Kinase II CaMKIIdelta/gamma does not affect ischemia/reperfusion (I/R) injury.
Cardiac CaM Kinase II genes delta and gamma contribute to adverse remodeling but redundantly inhibit calcineurin-induced myocardial hypertrophy.
CaMKIIdeltagamma couples noncanonical Wnt signaling to histone deacetylase 4 and myosin enhancer factor 2.
Camk2g-deficient obese mice have higher nuclear ATF6 (show ATF6 Proteins) levels, and silencing ATF6 (show ATF6 Proteins) in these mice lowers p58IPK (show DNAJC3 Proteins) and suppresses insulin (show INS Proteins)-induced p-Akt (show AKT1 Proteins).
Phosphorylation at specific PEVK/titin (show TTN Proteins) N2B-unique sequence sites was decreased in CAMK2g/d double knockout mice.
The CamkIIgamma isoform is poorly expressed in synaptic sites. Its activity is critical for receptor recycling and may provide a mechanism by which the postsynaptic acetylcholine receptor (show CHRNB1 Proteins) density is maintained at the neuromuscular junction in vivo.
The product of this gene is one of the four subunits of an enzyme which belongs to the serine/threonine protein kinase family, and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. In mammalian cells the enzyme is composed of four different chains: alpha, beta, gamma, and delta. The product of this gene is a gamma chain. Many alternatively spliced transcripts encoding different isoforms have been described but the full-length nature of all the variants has not been determined.
caMK-II subunit gamma
, calcium/calmodulin-dependent protein kinase (CaM kinase) II gamma
, calcium/calmodulin-dependent protein kinase type II subunit gamma
, caM kinase II subunit gamma
, caM-kinase II gamma chain
, calcium/calmodulin-dependent protein kinase type II gamma chain
, calcium/calmodulin-dependent protein kinase II gamma
, Ca2+/calmodulin-dependent protein kinase II
, CaMK II
, CaM kinase II gamma B
, CaM kinase II gamma C-1
, CaM kinase II gamma C-2
, CaM kinase II gamma G-1
, CaM kinase II gamma G-2
, CaM kinase II gamma J