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These findings uncover a direct mechanism of CaMKII (show CAMK2G Proteins) regulation by metabolism and further highlight the importance of metabolism in preserving oocyte viability.
analysis of metabolic regulation of CaMKII (show CAMK2G Proteins) protein and caspases in Xenopus laevis egg extracts
Characterization of a central Ca2 (show CA2 Proteins)+/calmodulin-dependent protein kinase (show CSNK1D Proteins) IIalpha/beta binding domain in densin that selectively modulates glutamate (show GRIN2A Proteins) receptor subunit phosphorylation.
This study demonstrate that this ASD (show ARSD Proteins)-linked de novo CAMK2A mutation disrupts multiple CaMKII (show CAMK2G Proteins) functions, induces synaptic deficits, and causes ASD (show ARSD Proteins)-related behavioral alterations.
CaMKII (show CAMK2G Proteins)-mediated recruitment and upregulation of CYLD (show CYLD Proteins) is expected to remove K63-linked polyubiquitins and facilitate proteasomal degradation at the postsynaptic density.
CAMK2A SNPs were associated with Alzheimer disease and mild cognitive impairment. AG genotype at the CAMK2A-rs3822606 was associated with AD risk.
CaMKII (show CAMK2G Proteins) phosphorylates SCN5A (show SCN5A Proteins) in vitro on 23 novel serine sites as was identified by mass spectrometry; reduced S516 phosphorylation has been found in human heart failure.
Ca2+/calmodulin-dependent protein kinase-II (CaMKII) has a key role in the plasticity of glutamatergic synapses of the brain.
we describe for the first time, two patients with MFD (show SCYL1 Proteins) and ID and for whom a deletion encompassing TCOF1 (show TCOF1 Proteins) and CAMK2A has been identified
a novel regulation of CaMKII (show CAMK2G Proteins) by another second messenger system and indicate its involvement in excitotoxic neuronal cell death.
Overexpression of a T253D phosphomimic form of calcium/calmodulin-dependent protein kinase type II subunit alpha significantly decreases proliferation, and cells accumulate in mitosis, specifically in metaphase.
results suggest that the CAMK2A gene may influence spatial and non-SWM performance in humans without any corresponding gross changes in frontal cortex or hippocampal anatomy.
found seven significant associations between CAMK2A SNPs and alcohol dependence, one of which in an autophosphorylation-related area of the gene.
Destabilization of PGC1a is attributable to decreased p38 MAPK (show MAPK14 Proteins) activation via diminished CaMKII (show CAMK2G Proteins) signaling. Thus, we elucidate a pathway downstream of Ca(2 (show CA2 Proteins)+)-mediated CaMKII (show CAMK2G Proteins) activation that is dysfunctional in C3KO(Capn3 (show CAPN3 Proteins) knock-out mice ) mice, leading to reduced transcription of genes involved in muscle adaptation
In young mice, 30% of adult CaMKIIalpha expression is sufficient for normal long-term potentiation in the hippocampus and cerebral cortex.
Findings demonstrate that Thr286 phosphorylation of CaMKII (show CAMK2G Proteins) plays an important role in induction of long-term potentiation (LTP (show SCP2 Proteins)) by integrating Ca(2 (show CA2 Proteins)+) signals, and it greatly promotes, but is dispensable for, the activation of CaMKII (show CAMK2G Proteins) and LTP (show SCP2 Proteins).
The present study demonstrates, for the first time, that ROS (show ROS1 Proteins)-dependent activation of CaMKII (show CAMK2G Proteins) mediates altered Ca2 (show CA2 Proteins)+ handling and contractile dysfunction observed in the setting of sepsis.
Thus, taken into consideration the mechanism that controls the upregulation of maturation genes involved in synaptic formation, these results indicate that Etv1 (show ETV1 Proteins) orchestrates the activity-dependent regulation of both maturation and immaturation genes in developing granule cells and plays a key role in specifying the identity of mature granule cells in the cerebellum.
Pharmacological and genetic studies using CaMKII (show CAMK2G Proteins) antagonists and genetically modified [alpha]-CaMKII (show CAMK2G Proteins) mice have shown that blockade or reduction of CaMKII (show CAMK2G Proteins) reduces nicotine reward
The study shows advanced glycation end products (AGEs) resulted from ribosylation activate calcium-/calmodulin-dependent protein kinase type II (CaMKII (show CAMK2G Proteins)), a key kinase responsible for Tau hyperphosphorylation.
HDAC2 (show HDAC2 Proteins) may regulate the expression of immediate early (show JUN Proteins) genes, in part, by prolonging the actions of pCREB in the mouse nucleus accumbens.
The results suggest that CaMKII (show CAMK2G Proteins)-dependent TnI (show TNNI2 Proteins) phosphorylation is involved in FDMCD and the consequent FDAR and that CaMKII (show CAMK2G Proteins) inhibition removes this mechanism and thus induces diastolic dysfunction.
Results indicate that alpha-Ca(2+)/calmodulin-dependent protein kinase II overexpression in the forebrain impairs behavioral flexibility and NMDAR (show GRIN1 Proteins)-dependent long-term depression in the medial prefrontal cortex.
We conclude that ouabain, even at low concentrations (0.5-8.0 mum), can increase INaL and reverse INCX , and these effects may contribute to the effect of the glycoside to increase Ca(2 (show CA2 Proteins)+) transients and contractility.
Data indicate that nitric oxide directly affects Ca-calmodulin (show CALM Proteins)-dependent protein kinase (show CDK7 Proteins) (CaMKII (show CAMK2G Proteins)) to sustain its activity leading to the increase in sarcoplasmic reticulum calcium leak.
Data indicate that the CaMKII (show CAMK2G Proteins) inhibitor, KN-93, can inhibit early afterdepolarizations (EADs), resulting in the suppression of torsades de pointes (TDP) induced by long-QT (LQT (show ARFGAP1 Proteins)) syndrome without affecting transmural dispersion of repolarization (TDR).
CaMKII (show CAMK2G Proteins) signaling, a crucial element of normal automaticity in rabbit sinoatrial node cells (SANC), is also involved in SANC bioenergetics.
The product of this gene belongs to the serine/threonine protein kinases family, and to the Ca(2+)/calmodulin-dependent protein kinases subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. This calcium calmodulin-dependent protein kinase is composed of four different chains: alpha, beta, gamma, and delta. The alpha chain encoded by this gene is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its calcium-calmodulin (CaM)-dependent activity, this protein can undergo autophosphorylation, resulting in CaM-independent activity. Two transcript variants encoding distinct isoforms have been identified for this gene.
calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha
, calcium/calmodulin-dependent protein kinase II beta
, calmodulin dependent protein kinase II beta subunit
, calcium/calmodulin-dependent protein kinase II alpha
, calcium/calmodulin-dependent protein kinase type II subunit alpha
, CaM kinase II alpha subunit
, CaM-kinase II alpha chain
, CaMK-II alpha subunit
, caM kinase II subunit alpha
, caMK-II subunit alpha
, calcium/calmodulin-dependent protein kinase II alpha-B subunit
, calcium/calmodulin-dependent protein kinase type II alpha chain
, CaMK II
, Ca2+/calmodulin-dependent protein kinase II alpha
, alpha CaM kinase II
, caM-kinase II alpha chain
, calcium/calmodulin-dependent protein kinase II alpha subunit
, calcium/calmodulin-dependent protein kinase type II alpha
, Calcium/calmodulin-dependent protein kinase type II alpha chain
, calcium/calmodulin-dependent protein kinase IIA