Browse our anti-CAMK2A (CAMK2A) Antibodies

Xenopus laevis Calcium/calmodulin-Dependent Protein Kinase II alpha (CAMK2A) interaction partners

1. These findings uncover a direct mechanism of CaMKII (show CAMK2G Antibodies) regulation by metabolism and further highlight the importance of metabolism in preserving oocyte viability.

2. analysis of metabolic regulation of CaMKII (show CAMK2G Antibodies) protein and caspases in Xenopus laevis egg extracts

3. Characterization of a central Ca2 (show CA2 Antibodies)+/calmodulin-dependent protein kinase (show CSNK1D Antibodies) IIalpha/beta binding domain in densin (show LRRC7 Antibodies) that selectively modulates glutamate (show GRIN2A Antibodies) receptor subunit phosphorylation.

Human Calcium/calmodulin-Dependent Protein Kinase II alpha (CAMK2A) interaction partners

1. The dynamics of calmodulin interactions with neurogranin (show NRGN Antibodies) and Ca(2 (show CA2 Antibodies)+) /CAMKII (show CAMK2G Antibodies) alpha proteins has been reported.

2. oxidative stress activates the TRPM2 (show CLU Antibodies)-Ca(2 (show CA2 Antibodies)+)-CAMK2 (show CAMK2B Antibodies) cascade to phosphorylate BECN1 (show BECN1 Antibodies) resulting in autophagy inhibition

3. two peptides (SIAPNV(-COOH) and SIVMNV(-COOH)) were identified to have considerably improved affinity with K d increase by ~tenfold relative to wild type peptide. Thus, the two peptides are considered as promising lead entities to develop therapeutic molecular agents with high efficacy and specificity to target CaMKIIalpha (show CAMK2 Antibodies)-MUPP1 (show MPDZ Antibodies) interaction.

4. The importance of CAMK2A and CAMK2B (show CAMK2B Antibodies) and their auto-phosphorylation in human brain function.

5. This study demonstrate that this ASD (show ARSD Antibodies)-linked de novo CAMK2A mutation disrupts multiple CaMKII (show CAMK2G Antibodies) functions, induces synaptic deficits, and causes ASD (show ARSD Antibodies)-related behavioral alterations.

6. CaMKII (show CAMK2G Antibodies)-mediated recruitment and upregulation of CYLD (show CYLD Antibodies) is expected to remove K63-linked polyubiquitins and facilitate proteasomal degradation at the postsynaptic density.

7. CAMK2A SNPs were associated with Alzheimer disease and mild cognitive impairment. AG genotype at the CAMK2A-rs3822606 was associated with AD risk.

8. CaMKII (show CAMK2G Antibodies) phosphorylates SCN5A (show SCN5A Antibodies) in vitro on 23 novel serine sites as was identified by mass spectrometry; reduced S516 phosphorylation has been found in human heart failure.

9. Ca2+/calmodulin-dependent protein kinase-II (CaMKII (show CAMK2 Antibodies)) has a key role in the plasticity of glutamatergic synapses of the brain.

10. we describe for the first time, two patients with MFD (show SCYL1 Antibodies) and ID and for whom a deletion encompassing TCOF1 (show TCOF1 Antibodies) and CAMK2A has been identified

Mouse (Murine) Calcium/calmodulin-Dependent Protein Kinase II alpha (CAMK2A) interaction partners

1. CaMKII (show CAMK2G Antibodies) is a target of PTENalpha phosphatase and that PTENalpha is an essential element in the molecular regulation of neural activity.

2. In FHC (show FTH1 Antibodies)-linked TnT (show TNNI1 Antibodies)-mutated hearts, RyR2 (show RYR2 Antibodies) is susceptible to CaMKII (show CAMK2G Antibodies)-mediated phosphorylation, presumably because of a mutation-linked increase in diastolic [Ca(2 (show CA2 Antibodies)+)]i, causing aberrant Ca(2 (show CA2 Antibodies)+) release leading to lethal arrhythmia.

3. astrocytic IL-17A (show IL17A Antibodies) plays important roles in the maintenance of neuropathic pain through CaMKII (show CAMK2G Antibodies)/CREB (show CREB1 Antibodies) signaling pathway in spinal cord.

4. Wip1 (show PPM1D Antibodies) phosphatase plays a vital role in regulating hippocampal synaptic plasticity by modulating the phosphorylation of CaMKII (show CAMK2G Antibodies).

5. Destabilization of PGC1a is attributable to decreased p38 MAPK (show MAPK14 Antibodies) activation via diminished CaMKII (show CAMK2G Antibodies) signaling. Thus, we elucidate a pathway downstream of Ca(2 (show CA2 Antibodies)+)-mediated CaMKII (show CAMK2G Antibodies) activation that is dysfunctional in C3KO(Capn3 (show CAPN3 Antibodies) knock-out mice ) mice, leading to reduced transcription of genes involved in muscle adaptation

6. In young mice, 30% of adult CaMKIIalpha (show CAMK2 Antibodies) expression is sufficient for normal long-term potentiation in the hippocampus and cerebral cortex.

7. Findings demonstrate that Thr286 phosphorylation of CaMKII (show CAMK2G Antibodies) plays an important role in induction of long-term potentiation (LTP (show SCP2 Antibodies)) by integrating Ca(2 (show CA2 Antibodies)+) signals, and it greatly promotes, but is dispensable for, the activation of CaMKII (show CAMK2G Antibodies) and LTP (show SCP2 Antibodies).

8. The present study demonstrates, for the first time, that ROS (show ROS1 Antibodies)-dependent activation of CaMKII (show CAMK2G Antibodies) mediates altered Ca2 (show CA2 Antibodies)+ handling and contractile dysfunction observed in the setting of sepsis.

9. Thus, taken into consideration the mechanism that controls the upregulation of maturation genes involved in synaptic formation, these results indicate that Etv1 (show ETV1 Antibodies) 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.

10. Pharmacological and genetic studies using CaMKII (show CAMK2G Antibodies) antagonists and genetically modified [alpha]-CaMKII (show CAMK2G Antibodies) mice have shown that blockade or reduction of CaMKII (show CAMK2G Antibodies) reduces nicotine reward

Rabbit Calcium/calmodulin-Dependent Protein Kinase II alpha (CAMK2A) interaction partners

1. 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 Antibodies)+) transients and contractility.

2. Data indicate that nitric oxide directly affects Ca-calmodulin-dependent protein kinase (show CDK7 Antibodies) (CaMKII (show CAMK2G Antibodies)) to sustain its activity leading to the increase in sarcoplasmic reticulum calcium leak.

3. Data indicate that the CaMKII (show CAMK2G Antibodies) inhibitor, KN-93, can inhibit early afterdepolarizations (EADs), resulting in the suppression of torsades de pointes (TDP) induced by long-QT (LQT (show ARFGAP1 Antibodies)) syndrome without affecting transmural dispersion of repolarization (TDR).

4. CaMKII (show CAMK2G Antibodies) signaling, a crucial element of normal automaticity in rabbit sinoatrial node cells (SANC), is also involved in SANC bioenergetics.