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These findings uncover a direct mechanism of CaMKII (show CAMK2G ELISA Kits) regulation by metabolism and further highlight the importance of metabolism in preserving oocyte viability.
analysis of metabolic regulation of CaMKII (show CAMK2G ELISA Kits) protein and caspases in Xenopus laevis egg extracts
Characterization of a central Ca2 (show CA2 ELISA Kits)+/calmodulin-dependent protein kinase (show CSNK1D ELISA Kits) IIalpha/beta binding domain in densin (show LRRC7 ELISA Kits) that selectively modulates glutamate (show GRIN2A ELISA Kits) receptor subunit phosphorylation.
The importance of CAMK2A and CAMK2B (show CAMK2B ELISA Kits) and their auto-phosphorylation in human brain function.
This study demonstrate that this ASD (show ARSD ELISA Kits)-linked de novo CAMK2A mutation disrupts multiple CaMKII (show CAMK2G ELISA Kits) functions, induces synaptic deficits, and causes ASD (show ARSD ELISA Kits)-related behavioral alterations.
CaMKII (show CAMK2G ELISA Kits)-mediated recruitment and upregulation of CYLD (show CYLD ELISA Kits) 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 ELISA Kits) phosphorylates SCN5A (show SCN5A ELISA Kits) 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 (show CAMK2 ELISA Kits)) 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 ELISA Kits) and ID and for whom a deletion encompassing TCOF1 (show TCOF1 ELISA Kits) and CAMK2A has been identified
a novel regulation of CaMKII (show CAMK2G ELISA Kits) 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.
Destabilization of PGC1a (show PPARGC1A ELISA Kits) is attributable to decreased p38 MAPK (show MAPK14 ELISA Kits) activation via diminished CaMKII (show CAMK2G ELISA Kits) signaling. Thus, we elucidate a pathway downstream of Ca(2 (show CA2 ELISA Kits)+)-mediated CaMKII (show CAMK2G ELISA Kits) activation that is dysfunctional in C3KO(Capn3 (show CAPN3 ELISA Kits) knock-out mice ) mice, leading to reduced transcription of genes involved in muscle adaptation
In young mice, 30% of adult CaMKIIalpha (show CAMK2 ELISA Kits) expression is sufficient for normal long-term potentiation in the hippocampus and cerebral cortex.
Findings demonstrate that Thr286 phosphorylation of CaMKII (show CAMK2G ELISA Kits) plays an important role in induction of long-term potentiation (LTP (show SCP2 ELISA Kits)) by integrating Ca(2 (show CA2 ELISA Kits)+) signals, and it greatly promotes, but is dispensable for, the activation of CaMKII (show CAMK2G ELISA Kits) and LTP (show SCP2 ELISA Kits).
The present study demonstrates, for the first time, that ROS (show ROS1 ELISA Kits)-dependent activation of CaMKII (show CAMK2G ELISA Kits) mediates altered Ca2 (show CA2 ELISA Kits)+ 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 ELISA Kits) 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 ELISA Kits) antagonists and genetically modified [alpha]-CaMKII (show CAMK2G ELISA Kits) mice have shown that blockade or reduction of CaMKII (show CAMK2G ELISA Kits) 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 ELISA Kits)), a key kinase responsible for Tau hyperphosphorylation.
HDAC2 (show HDAC2 ELISA Kits) may regulate the expression of immediate early (show JUN ELISA Kits) genes, in part, by prolonging the actions of pCREB in the mouse nucleus accumbens.
The results suggest that CaMKII (show CAMK2G ELISA Kits)-dependent TnI (show TNNI2 ELISA Kits) phosphorylation is involved in FDMCD and the consequent FDAR and that CaMKII (show CAMK2G ELISA Kits) inhibition removes this mechanism and thus induces diastolic dysfunction.
Results indicate that alpha-Ca(2+)/calmodulin-dependent protein kinase II (show CAMK2 ELISA Kits) overexpression in the forebrain impairs behavioral flexibility and NMDAR (show GRIN1 ELISA Kits)-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 ELISA Kits)+) transients and contractility.
Data indicate that nitric oxide directly affects Ca-calmodulin-dependent protein kinase (show CDK7 ELISA Kits) (CaMKII (show CAMK2G ELISA Kits)) to sustain its activity leading to the increase in sarcoplasmic reticulum calcium leak.
Data indicate that the CaMKII (show CAMK2G ELISA Kits) inhibitor, KN-93, can inhibit early afterdepolarizations (EADs), resulting in the suppression of torsades de pointes (TDP) induced by long-QT (LQT (show ARFGAP1 ELISA Kits)) syndrome without affecting transmural dispersion of repolarization (TDR).
CaMKII (show CAMK2G ELISA Kits) 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