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anti-Human CAMK2A Antibodies:
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Rat (Rattus) Polyclonal CAMK2A Primary Antibody for WB - ABIN361458
Ahmed, Gardiner: Preserving protein profiles in tissue samples: differing outcomes with and without heat stabilization. in Journal of neuroscience methods 2011
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Mouse (Murine) Polyclonal CAMK2A Primary Antibody for WB - ABIN152527
Hudmon, Schulman: Neuronal CA2+/calmodulin-dependent protein kinase II: the role of structure and autoregulation in cellular function. in Annual review of biochemistry 2002
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Dog (Canine) Monoclonal CAMK2A Primary Antibody for BI, IF - ABIN968457
Brocke, Chiang, Wagner, Schulman: Functional implications of the subunit composition of neuronal CaM kinase II. in The Journal of biological chemistry 1999
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Dog (Canine) Monoclonal CAMK2A Primary Antibody for BI, IF - ABIN968458
Fallon, Moreau, Croft, Labib, Gu, Fon: Parkin and CASK/LIN-2 associate via a PDZ-mediated interaction and are co-localized in lipid rafts and postsynaptic densities in brain. in The Journal of biological chemistry 2002
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Rat (Rattus) Monoclonal CAMK2A Primary Antibody for ICC, IF - ABIN151484
George, Baden, Gerwick, Murray: Bidirectional influence of sodium channel activation on NMDA receptor-dependent cerebrocortical neuron structural plasticity. in Proceedings of the National Academy of Sciences of the United States of America 2012
Show all 4 Pubmed References
Rat (Rattus) Monoclonal CAMK2A Primary Antibody for ICC, IF - ABIN451525
Jiang, Xu, Song, Li, Mao, Zhao, He, Yang, Dai: Calmodulin-dependent protein kinase II/cAMP response element-binding protein/Wnt/β-catenin signaling cascade regulates angiotensin II-induced podocyte injury and albuminuria. in The Journal of biological chemistry 2013
Show all 2 Pubmed References
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.
analysis of metabolic regulation of CaMKII (show CAMK2G Antibodies) protein and caspases in Xenopus laevis egg extracts
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.
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.
The importance of CAMK2A and CAMK2B (show CAMK2B Antibodies) and their auto-phosphorylation in human brain function.
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.
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.
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 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.
Ca2+/calmodulin-dependent protein kinase-II (CaMKII (show CAMK2 Antibodies)) 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 Antibodies) and ID and for whom a deletion encompassing TCOF1 (show TCOF1 Antibodies) and CAMK2A has been identified
a novel regulation of CaMKII (show CAMK2G Antibodies) 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.
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.
Wip1 (show PPM1D Antibodies) phosphatase plays a vital role in regulating hippocampal synaptic plasticity by modulating the phosphorylation of CaMKII (show CAMK2G Antibodies).
Destabilization of PGC1a (show PPARGC1A Antibodies) 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
In young mice, 30% of adult CaMKIIalpha (show CAMK2 Antibodies) expression is sufficient for normal long-term potentiation in the hippocampus and cerebral cortex.
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).
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.
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.
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
The study shows advanced glycation end products (AGEs) resulted from ribosylation activate calcium-/calmodulin-dependent protein kinase type II (CaMKII (show CAMK2G Antibodies)), a key kinase responsible for Tau hyperphosphorylation.
HDAC2 (show HDAC2 Antibodies) may regulate the expression of immediate early (show JUN Antibodies) genes, in part, by prolonging the actions of pCREB in the mouse nucleus accumbens.
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.
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.
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).
CaMKII (show CAMK2G Antibodies) 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