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. Study first demonstrated that CaMKII (show CAMK2G Antibodies)-alpha was over-expressed in human colon cancers and was associated with cancer differentiation.

2. 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.

3. 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

4. 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.

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

6. 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.

7. 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.

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

9. 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.

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

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

1. Study showed the significance of TLR4 (show TLR4 Antibodies) in upregulation of MAPK/ErK (show MAPK1 Antibodies) in NMDAR (show GRIN1 Antibodies) hypofunction schizophrenic-mouse model. This is characterized by a decrease in hippocampal IGF-1R (show IGF1R Antibodies)/CaMKIIalpha (show CAMK2 Antibodies), and social interaction behavioral deficits. Ultimately, hippocampal TLR4 (show TLR4 Antibodies) knockdown rescued IGF-1R (show IGF1R Antibodies)/CaMKIIalpha (show CAMK2 Antibodies) decline and prevented behavioral deficits by reducing MAPK/ErK (show MAPK1 Antibodies) expression.

2. Hyperlipidemia induced by a high-fat diet was associated with increased expression and activity of CaMKII (show CAMK2G Antibodies) in heart.

3. Data show that calcium/calmodulin protein kinase (show CDK7 Antibodies) II (CaMKII (show CAMK2G Antibodies))-mediated modulation of neuronal sodium current impacts neuronal excitability in SCN2A (show SCN2A Antibodies) sodium channel alpha subunit (show SCN4A Antibodies) Scn2a (show SCN2A Antibodies)(Q54) mice and may represent a therapeutic target for the treatment of epilepsy.

4. Results show that aging impairs the training-induced upregulation of autophosphorylated (T286) alphaCaMKII in the CA3 (show CA3 Antibodies) stratum radiatum of the hippocampus. This indicates that distinct age-related mechanisms underlie CFC (show TBCC Antibodies) that may rely more heavily on NMDA receptor-dependent plasticity in young age.

5. This study found that the Camk2a gene showed a downregulated profile only in the Inflexible when compared to the Light ethanol drinkers group.

6. Results suggest that the increased expression of calcium/calmodulin dependent protein kinase II (show CAMK2 Antibodies) in the lateral habenula is instrumental for morphine-driven aversive behaviors.

7. our findings demonstrated that TINCR could attenuate myocardial hypertrophy by epigenetically silencing of CaMKII (show CAMK2G Antibodies), which may provide a novel therapeutic strategy for cardiac hypertrophy.

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

9. 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.

10. 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.

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.