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anti-Human CAMK2G Antikörper:
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Human CAMK2G Primary Antibody für IHC - ABIN965740
Pak, Huang, Li, Balschun, Reymann, Chiang, Westphal, Huang: Involvement of neurogranin in the modulation of calcium/calmodulin-dependent protein kinase II, synaptic plasticity, and spatial learning: a study with knockout mice. in Proceedings of the National Academy of Sciences of the United States of America 2000
Human Polyclonal CAMK2G Primary Antibody für IF, WB - ABIN362984
Bossuyt, Helmstadter, Wu, Clements-Jewery, Haworth, Avkiran, Martin, Pogwizd, Bers: Ca2+/calmodulin-dependent protein kinase IIdelta and protein kinase D overexpression reinforce the histone deacetylase 5 redistribution in heart failure. in Circulation research 2008
Cow (Bovine) Monoclonal CAMK2G Primary Antibody für ICC, IF - ABIN361644
Barria, Muller, Derkach, Griffith, Soderling: Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation. in Science (New York, N.Y.) 1997
Show all 13 Pubmed References
Human Monoclonal CAMK2G Primary Antibody für ICC, IF - ABIN361699
Bennett, Kennedy: Deduced primary structure of the beta subunit of brain type II Ca2+/calmodulin-dependent protein kinase determined by molecular cloning. in Proceedings of the National Academy of Sciences of the United States of America 1987
Show all 14 Pubmed References
Human Polyclonal CAMK2G Primary Antibody für IHC (p), WB - ABIN391313
Tombes, Krystal: Identification of novel human tumor cell-specific CaMK-II variants. in Biochimica et biophysica acta 1997
Show all 2 Pubmed References
The data further showed that mitochondrial fission significantly promoted the reprogramming of focal-adhesion dynamics and lamellipodia formation in hepatocellular carcinoma cells mainly by activating typical Ca(2+) /CaMKII/ERK/FAK pathway.
Subunit exchange enhances information retention by CaMKII in dendritic spines.
point mutation R292P sufficient to disrupt gene expression and spatial learning
The effect of Ca(2+), domain-specificity, and CaMKII on CaM binding to NaV1.1 has been reported.
The data suggest T287 autophosphorylation regulates substrate gating, an intrinsic property of the catalytic domain, which is amplified within the multivalent architecture of the calcium/calmodulin-dependent protein kinase II holoenzyme.
These findings indicate that the CaMKII-mediated GluA1 phosphorylation of S567 and S831 is critical for P2X2-mediated AMPAR internalization and ATP-driven synaptic depression.
Laminin is instructive and CaMKII is non-permissive for the formation of complex aggregates of acetylcholine receptors on myotubes in culture.
A new molecular mechanism mediated by CAMK2gamma in intestinal epithelial cells during colitis-associated cancer (CAC) development, thereby providing a potential new therapeutic target for CAC.
oxidative stress activated the TRPM2-CaMKII cascade to further induce intracellular ROS production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
novel mechanism by which CAMK2gamma antagonizes mTORC1 activation during hepatocarcinogenesis
CKIalpha-mediated NS5A S235 phosphorylation is critical for HCV replication. CaMKII gamma and delta may have negative roles in the HCV life cycle.
Demonstrate that calcium/CaMKIIgamma/AKT signaling can regulate apoptosis and autophagy simultaneously in colorectal cancer cells.
High CaMKIIgamma expression is associated with lung cancer.
Dysfunction in CaMKII-based signaling has been linked with a host of cardiovascular phenotypes including heart failure and arrhythmia, and CaMKII levels are elevated in human and animal disease models of heart disease.
Inhibition of CaMKII activity results in an upregulation of CaMKIV mRNA and protein in leukemia cell lines.
CAMKIIgamma, HSP70 and HSP90 transcripts are differentially expressed in chronic myeloid leukemia cells from patients with resistant mutated disease.
CaMKII-dependent microtube polymerization may be responsible for the enhanced uptake of PEI/ON complexes in A549 cells under oxidative stress conditions.
Our data suggest that berbamine and its derivatives are promising agents to suppress liver cancer growth by targeting CAMKII
CaMKII overexpression in mushroom body neurons increases activity dependent calcium responses.
it can be concluded that CaMKII regulates the activity of ASIC1, which is associated with the ability of GBM cells to migrate.
Redox-sensitive activation of p38 MAPK/HSP27 pathway or ERK1/2 in endothelial cells requires CaMKII
critical for long-term potentiation and spatial learning
Data, including data from studies using transgenic mice, suggest that signaling via prostaglandin-F2alpha/PTGFR and Camk2g/p38/Foxo1 MAP kinase/calcium pathways are involved in regulation of hepatic gluconeogenesis in both obesity and fasting. (Ptgfr = prostaglandin F2alpha receptor; Camk2g = calcium-calmodulin-dependent protein kinase type 2 gamma; p38 = p38 MAP kinase; Foxo1 = forkhead box transcription factor O1)
RGS6 and oxidized CaMKIIdelta together function as novel critical upstream modulators of Notch signaling required for normal cardiovascular development and embryo survival.
CaMKIIgamma-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIgamma had increased expression of the transcription factor ATF6.
Data indicate that combined cardiomyocyte-specific deletion of CaM Kinase II CaMKIIdelta/gamma does not affect ischemia/reperfusion (I/R) injury.
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.
Camk2g-deficient obese mice have higher nuclear ATF6 levels, and silencing ATF6 in these mice lowers p58IPK and suppresses insulin-induced p-Akt.
Phosphorylation at specific PEVK/titin N2B-unique sequence sites was decreased in CAMK2g/d double knockout mice.
The present study provides support for BAD-Ser170 phosphorylation playing a key role not only in regulating BAD's pro-apoptotic activity, but also in cell proliferation.
The CamkIIgamma isoform is poorly expressed in synaptic sites. Its activity is critical for receptor recycling and may provide a mechanism by which the postsynaptic acetylcholine receptor density is maintained at the neuromuscular junction in vivo.
Data suggest that CaMKIIgamma specifically controls mouse egg activation by regulating cell cycle resumption.
CamKIIgamma3 isoform plays a necessary and sufficient role in transducing the oscillatory Ca(2+) signal into cell cycle resumption, but not into cortical granule release
These data support an integrated model in which CaMKII serves as a unifying link between ER stress and the Fas and mitochondrial apoptotic pathways.
role in cell communication
Our results suggest that absence of adequate Ca2+signaling through nuclear CaMKII regulated pathways leads to development of cardiac disease.
CaMKI/IIgamma have roles in osteoclast differentiation and bone resportion via RANKL.
plays a role in calcium signaling. (review)
The product of this gene is one of the four subunits of an enzyme which 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 gamma chain. Many alternatively spliced transcripts encoding different isoforms have been described but the full-length nature of all the variants has not been determined.
caMK-II subunit gamma
, calcium/calmodulin-dependent protein kinase (CaM kinase) II gamma
, calcium/calmodulin-dependent protein kinase type II subunit gamma
, caM kinase II subunit gamma
, caM-kinase II gamma chain
, calcium/calmodulin-dependent protein kinase type II gamma chain
, calcium/calmodulin-dependent protein kinase II gamma
, Ca2+/calmodulin-dependent protein kinase II
, CaMK II
, CaM kinase II gamma B
, CaM kinase II gamma C-1
, CaM kinase II gamma C-2
, CaM kinase II gamma G-1
, CaM kinase II gamma G-2
, CaM kinase II gamma J