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anti-Human CAMK2D Antikörper:
anti-Rat (Rattus) CAMK2D Antikörper:
anti-Mouse (Murine) CAMK2D Antikörper:
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Rat (Rattus) Polyclonal CAMK2D Primary Antibody für IHC (fro), WB - ABIN548999
Matsumoto, Ebihara, Yamamoto, Tabuchi, Fukunaga, Yasunami, Ohkubo, Shichiri, Miyamoto: Cloning from insulinoma cells of synapsin I associated with insulin secretory granules. in The Journal of biological chemistry 1999
Show all 5 Pubmed References
Human Polyclonal CAMK2D Primary Antibody für IHC (p), ELISA - ABIN543735
Hoch, Meyer, Hetzer, Krause, Karczewski: Identification and expression of delta-isoforms of the multifunctional Ca2+/calmodulin-dependent protein kinase in failing and nonfailing human myocardium. in Circulation research 1999
Show all 3 Pubmed References
CKIalpha-mediated NS5A S235 phosphorylation is critical for HCV replication. CaMKII gamma and delta may have negative roles in the HCV life cycle.
TGFbeta elevated the expression of CamK IIbeta and CamK IIdelta, while siRNA silencing of those two subtypes significantly reduced TGFbeta-mediated expression of collagen A1 and fibronectin 1.
CEACAM1 is able to maintain the active transcription of ID4 by an epigenetic mechanism involving HDAC4 and CaMK2D, and the same kinase enables lumen formation by CEACAM1
CaMKIId activity is up-regulated in the myocardium of diabetic patients and mouse models of diabetes, where it promotes pathological signaling that includes hypertrophy, fibrosis and apoptosis.
Study found a significant association with disordered gambling and rs167771 (DRD3) and with rs381572 (CAMK2D) in humans
This study showed that AKAP12,CAMK2D and a molecular pathway(cyclic amp)association to outcome of depressive during citalopram treatment.
Reveal a novel in vivo function of CaMKIIdelta in regulating H3 phosphorylation and suggest a novel epigenetic mechanism by which CaMKIIdelta controls cardiac hypertrophy.
CaMKIID specifically phosphorylates Thr-457 on CEACAM1-SF, which in turn regulates the process of lumen formation via apoptosis of the central acinar cells.
CAMKIIdelta is required for PP1gamma-exacerbated apoptosis of cardiomyocytes.
Our studies suggest that CaMKII is a molecular signal that couples increased reactive oxygen species with atrial fibrillation and that therapeutic strategies to decrease oxidized CaMKII may prevent or reduce it.
End-stage failing human hearts had more phosphorylation at CaMKII-dependent titin sites, contributing to their mechanical dysfunction & establishing a new role for CaMKIIdelta in regulating diastolic passive properties of healthy & diseased hearts.
suggest that CaMKII and calcineurin provide a switch-like mechanism that controls Ca-dependent LIMK1, SSH1L and cofilin activation, and subsequently actin cytoskeletal reorganization
Data show that Pcp4 overexpression induces precocious neuronal differentiation, and is associated with an increase in CaMKIIdelta activation.
Single nucleotide polymorphism in CAMK2D gene is associated with epithelial ovarian cancer.
This study shows for the first time that CAMKII inhibition acutely improves contractility in human heart failure where CAMKIIdelta expression is increased.
The crystal structure of the human CaMKIIdelta/Ca2+/CaM complex, is described.
Calcium/Calmodulin-dependent protein kinase II delta 6 (CaMKIIdelta6) and RhoA is involved in thrombin-induced endothelial barrier dysfunction
role in cell communication
measured differences in CaMKII binding affinities for CaM play a minor role in the autophosphorylation of the enzyme, largely dictated by autophosphorylation rate for alpha, beta, gamma and delta isoforms
HDAC4 as a specific downstream substrate of CaMKIIdeltaB in cardiac cells and have broad applications for the signaling pathways leading to cardiac hypertrophy and heart failure.
CaMKIIdelta isoforms have similar effects on hypertrophic gene expression but disparate effects on Ca(2+) handling
surgical-induced Osteoarthritis mice treated with a miR-146a inhibitor significantly alleviated the destruction of articular cartilage via targeting Camk2d and Ppp3r2.
we demonstrate that the deltaC isoform of CaMKII contributes significantly to myocardial damage following ex vivo I/R. Signaling occurs through NF-kappaB and TNF-alpha and acute inhibition of the generation or function of thesemolecules has a very robust protective effect inWT animals and in those expressing CaMKIIdeltaC.
Phosphorylating Titin's Cardiac N2B Element by ERK2 or CaMKIIdelta Lowers the Single Molecule and Cardiac Muscle Force
CaMK2d-dependent phosphorylation of RyR2-S2814 is significant in cardiomyopathy, independent of hypertrophy, induced by prolonged beta-adrenergic receptor stimulation.
Data indicate that combined cardiomyocyte-specific deletion of CaM Kinase II CaMKIIdelta/gamma does not affect ischemia/reperfusion (I/R) injury.
CaMKIIdelta activation and phosphorylation of downstream targets was enhanced in aromatase knockout hearts subjected to ischemia-reperfusion
Oxidative stress was elevated in mitochondria from Gq versus wild-type mice and respiratory rates were lower; these changes in mitochondrial function were restored by CaMKIIdelta deletion.
Cardiac CaM Kinase II genes delta and gamma contribute to adverse remodeling but redundantly inhibit calcineurin-induced myocardial hypertrophy.
CaMKIIdeltagamma couples noncanonical Wnt signaling to histone deacetylase 4 and myosin enhancer factor 2.
developed an ionic model of the ventricular myocyte to interrogate potentially arrhythmogenic positive feedback in both control conditions and when CaMKIIdeltaC is overexpressed
we show selective upregulation of CaMKIIdelta in adult cardiac fibroblasts following cardiac hypertrophy and assign a previously unrecognised role to CaMKII in regulating adult cardiac fibroblast function in normal and diseased mouse hearts.
Camk2d expression and activity increase during arteriogenesis
CaMKII activation may not be required for abnormal impulse induction in stretched ventricular myocytes.
can be phosphoryalated by CaMKIId, both in vitro and in vivo.
Activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction.
Phosphorylation at specific PEVK/titin N2B-unique sequence sites was decreased in CAMK2g/d double knockout mice.
CaMKIIdelta exhibited consistent expression patterns between its mRNA and protein with both rising remarkably during osteoclastogenesis
These results demonstrate that there are dramatic CaMKII-mediated effects on RyR Calcium release that occur via regulation of both RyR activation and termination processes.
A specific inhibitor of CaMKII can effectively inhibit the occurrence of EADs.
The product of this gene belongs to the serine/threonine protein kinase family and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. In mammalian cells, the enzyme is composed of four different chains: alpha, beta, gamma, and delta. The product of this gene is a delta chain. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Distinct isoforms of this chain have different expression patterns.
CaM kinase II delta subunit
, CaM-kinase II delta chain
, CaMK-II delta subunit
, caM kinase II subunit delta
, caMK-II subunit delta
, calcium/calmodulin-dependent protein kinase (CaM kinase) II delta
, calcium/calmodulin-dependent protein kinase type II delta chain
, calcium/calmodulin-dependent protein kinase type II subunit delta
, caM-kinase II delta chain
, Ca++/calmodulin-dependent protein kinase 2 delta subunit
, Ca++/calmodulin-dependent protein kinase II delta subunit
, Ca++/calmodulin-dependent protein kinase II, delta subunit
, calcium/calmodulin-dependent protein kinase II delta 2-subunit
, calcium/calmodulin-dependent protein kinase II delta12 subunit
, calcium/calmodulin-dependent protein kinase II, delta
, calcium/calmodulin-dependent protein kinase II delta
, CaMK II