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These findings uncover a direct mechanism of CaMKII (zeige CAMK2G Proteine) regulation by metabolism and further highlight the importance of metabolism in preserving oocyte viability.
analysis of metabolic regulation of CaMKII (zeige CAMK2G Proteine) protein and caspases in Xenopus laevis egg extracts
Characterization of a central Ca2 (zeige CA2 Proteine)+/calmodulin-dependent protein kinase (zeige CSNK1D Proteine) IIalpha/beta binding domain in densin that selectively modulates glutamate (zeige GRIN2A Proteine) receptor subunit phosphorylation.
The importance of CAMK2A and CAMK2B (zeige CAMK2B Proteine) and their auto-phosphorylation in human brain function.
This study demonstrate that this ASD (zeige ARSD Proteine)-linked de novo CAMK2A mutation disrupts multiple CaMKII (zeige CAMK2G Proteine) functions, induces synaptic deficits, and causes ASD (zeige ARSD Proteine)-related behavioral alterations.
CaMKII (zeige CAMK2G Proteine)-mediated recruitment and upregulation of CYLD (zeige CYLD Proteine) 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 (zeige CAMK2G Proteine) phosphorylates SCN5A (zeige SCN5A Proteine) 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 (zeige SCYL1 Proteine) and ID and for whom a deletion encompassing TCOF1 (zeige TCOF1 Proteine) and CAMK2A has been identified
a novel regulation of CaMKII (zeige CAMK2G Proteine) 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 is attributable to decreased p38 MAPK (zeige MAPK14 Proteine) activation via diminished CaMKII (zeige CAMK2G Proteine) signaling. Thus, we elucidate a pathway downstream of Ca(2 (zeige CA2 Proteine)+)-mediated CaMKII (zeige CAMK2G Proteine) activation that is dysfunctional in C3KO(Capn3 (zeige CAPN3 Proteine) 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 (zeige CAMK2G Proteine) plays an important role in induction of long-term potentiation (LTP (zeige SCP2 Proteine)) by integrating Ca(2 (zeige CA2 Proteine)+) signals, and it greatly promotes, but is dispensable for, the activation of CaMKII (zeige CAMK2G Proteine) and LTP (zeige SCP2 Proteine).
The present study demonstrates, for the first time, that ROS (zeige ROS1 Proteine)-dependent activation of CaMKII (zeige CAMK2G Proteine) mediates altered Ca2 (zeige CA2 Proteine)+ 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 (zeige ETV1 Proteine) 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 (zeige CAMK2G Proteine) antagonists and genetically modified [alpha]-CaMKII (zeige CAMK2G Proteine) mice have shown that blockade or reduction of CaMKII (zeige CAMK2G Proteine) reduces nicotine reward
The study shows advanced glycation end products (AGEs) resulted from ribosylation activate calcium-/calmodulin-dependent protein kinase type II (CaMKII (zeige CAMK2G Proteine)), a key kinase responsible for Tau hyperphosphorylation.
HDAC2 (zeige HDAC2 Proteine) may regulate the expression of immediate early (zeige JUN Proteine) genes, in part, by prolonging the actions of pCREB in the mouse nucleus accumbens.
The results suggest that CaMKII (zeige CAMK2G Proteine)-dependent TnI (zeige TNNI2 Proteine) phosphorylation is involved in FDMCD and the consequent FDAR and that CaMKII (zeige CAMK2G Proteine) 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 (zeige GRIN1 Proteine)-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 (zeige CA2 Proteine)+) transients and contractility.
Data indicate that nitric oxide directly affects Ca-calmodulin-dependent protein kinase (zeige CDK7 Proteine) (CaMKII (zeige CAMK2G Proteine)) to sustain its activity leading to the increase in sarcoplasmic reticulum calcium leak.
Data indicate that the CaMKII (zeige CAMK2G Proteine) inhibitor, KN-93, can inhibit early afterdepolarizations (EADs), resulting in the suppression of torsades de pointes (TDP) induced by long-QT (LQT (zeige ARFGAP1 Proteine)) syndrome without affecting transmural dispersion of repolarization (TDR).
CaMKII (zeige CAMK2G Proteine) 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