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 regulation by metabolism and further highlight the importance of metabolism in preserving oocyte viability.

2. analysis of metabolic regulation of CaMKII protein and caspases in Xenopus laevis egg extracts

3. Characterization of a central Ca2+/calmodulin-dependent protein kinase IIalpha/beta binding domain in densin that selectively modulates glutamate receptor subunit phosphorylation.

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

1. Together, these data demonstrate that a recessive germline mutation in CAMK2A leads to neurodevelopmental defects in humans and suggest that dysfunctional CAMK2 paralogs may contribute to other neurological disorders.

2. We correlated the self-reported time interval between occasional and regular heroin use with the frequency of 12 single nucleotide polymorphisms located within the genomic region of the CamK2A gene. Single marker association analysis (rs10066581, P=0.007), as well as haplotype analysis (global P=0.005), suggested an association with the quantitative trait 'time interval from occasional to regular heroin use.

3. SK current is increased via the enhanced activation of CaMKII in patients with atrial fibrillation.

4. Study first demonstrated that CaMKII-alpha was over-expressed in human colon cancers and was associated with cancer differentiation.

5. The dynamics of calmodulin interactions with neurogranin and Ca(2+) /CAMKII alpha proteins has been reported.

6. oxidative stress activates the TRPM2-Ca(2+)-CAMK2 cascade to phosphorylate BECN1 resulting in autophagy inhibition

7. 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-MUPP1 interaction.

8. The importance of CAMK2A and CAMK2B and their auto-phosphorylation in human brain function.

9. This study demonstrate that this ASD-linked de novo CAMK2A mutation disrupts multiple CaMKII functions, induces synaptic deficits, and causes ASD-related behavioral alterations.

10. CaMKII-mediated recruitment and upregulation of CYLD is expected to remove K63-linked polyubiquitins and facilitate proteasomal degradation at the postsynaptic density.

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

12. CaMKII phosphorylates SCN5A in vitro on 23 novel serine sites as was identified by mass spectrometry; reduced S516 phosphorylation has been found in human heart failure.

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

14. we describe for the first time, two patients with MFD and ID and for whom a deletion encompassing TCOF1 and CAMK2A has been identified

15. a novel regulation of CaMKII by another second messenger system and indicate its involvement in excitotoxic neuronal cell death.

16. 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.

17. 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.

18. found seven significant associations between CAMK2A SNPs and alcohol dependence, one of which in an autophosphorylation-related area of the gene.

19. These results suggest that Osterix is a novel target of CaMKII and the activity of Osterix can be modulated by a novel mechanism involving CaMKII during osteoblast differentiation.

20. Rem2 has a role in neuronal plasticity hrough co-trafficking with CaMKIIa

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

1. It has been suggested that calcium release from presynaptic endoplasmic reticulum activates CaMKII which, in turn, facilitates the mobilization and secretion of large dense-core vesicles.

2. Cardiac specific PRMT1 ablation causes heart failure through CaMKII dysregulation

3. Fluorescence resonance energy transfer studies confirm that the extended state of CaMKII-alpha resolved by electron microscopy is the predominant form of the holoenzyme, even under molecular crowding conditions.

4. Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model.

5. Its pathway may promote reactive oxygen species generation in the early state Alzheimer's disease and eventually contribute to the exacerbation of pathological phenotype.

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

7. Hyperlipidemia induced by a high-fat diet was associated with increased expression and activity of CaMKII in heart.

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

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

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

11. Results suggest that the increased expression of calcium/calmodulin dependent protein kinase II in the lateral habenula is instrumental for morphine-driven aversive behaviors.

12. our findings demonstrated that TINCR could attenuate myocardial hypertrophy by epigenetically silencing of CaMKII, which may provide a novel therapeutic strategy for cardiac hypertrophy.

13. CaMKII is a target of PTENalpha phosphatase and that PTENalpha is an essential element in the molecular regulation of neural activity.

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

15. Data suggest that alphaCaMKII autophosphorylation-dependent remodeling of glutamatergic synapses is a plausible mechanism for the regulation of the alcohol addiction-related behaviors.

16. astrocytic IL-17A plays important roles in the maintenance of neuropathic pain through CaMKII/CREB signaling pathway in spinal cord.

17. Wip1 phosphatase plays a vital role in regulating hippocampal synaptic plasticity by modulating the phosphorylation of CaMKII.

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

19. In young mice, 30% of adult CaMKIIalpha expression is sufficient for normal long-term potentiation in the hippocampus and cerebral cortex.

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

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+) transients and contractility.

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

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

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