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anti-Human CAMK4 Antibodies:
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Human Monoclonal CAMK4 Primary Antibody for IF, IP - ABIN967875
Ohmstede, Bland, Merrill, Sahyoun: Relationship of genes encoding Ca2+/calmodulin-dependent protein kinase Gr and calspermin: a gene within a gene. in Proceedings of the National Academy of Sciences of the United States of America 1991
Show all 5 Pubmed References
Human Monoclonal CAMK4 Primary Antibody for IF, IP - ABIN967876
Passier, Zeng, Frey, Naya, Nicol, McKinsey, Overbeek, Richardson, Grant, Olson: CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo. in The Journal of clinical investigation 2000
Show all 5 Pubmed References
Human Monoclonal CAMK4 Primary Antibody for ICC, FACS - ABIN1098144
Dias, Cheung, Wang, Hart: Regulation of calcium/calmodulin-dependent kinase IV by O-GlcNAc modification. in The Journal of biological chemistry 2009
Show all 2 Pubmed References
Human Polyclonal CAMK4 Primary Antibody for IHC, IHC (p) - ABIN4287591
Harrison, Flight, Gomes, Venkat, Ellis, Sankar, Twiss, Rouchka, Petruska: IB4-binding sensory neurons in the adult rat express a novel 3' UTR-extended isoform of CaMK4 that is associated with its localization to axons. in The Journal of comparative neurology 2013
Human Monoclonal CAMK4 Primary Antibody for IF, IHC (p) - ABIN560153
Nakanishi, Hata, Nagayama, Sakurai, Nishisho, Wakabayashi, Hiraga, Ebisu, Yoneda: Acid activation of Trpv1 leads to an up-regulation of calcitonin gene-related peptide expression in dorsal root ganglion neurons via the CaMK-CREB cascade: a potential mechanism of inflammatory pain. in Molecular biology of the cell 2010
hTau accumulation impairs synapse and memory by CaN-mediated suppression of nuclear CaMKIV/CREB (show CREB1 Antibodies) signaling.
Within the pH range 5.0-11.5, CAMK4 maintained both its secondary and tertiary structures, along with its function, whereas significant aggregation was observed at acidic pH (2.0-4.5).
A positive association was not observed between rs10491334 in the CAMK4 gene and longevity in a Chinese population.
The T-allele of rs10491334 in CAMK4 was associated with hypertension in the Uygur group.
Expression of CaMKIV inhibits autophosphorylation and activation of CaMKII (show CAMK2G Antibodies), and elicits G0/G1cell cycle arrest,impairing cell proliferation.
An imbalance of specific isoforms of CYFIP1 (show CYFIP1 Antibodies), an FMRP (show FMR1 Antibodies) interaction partner, and CAMK4, a transcriptional regulator of the FMRP (show FMR1 Antibodies) gene, modulates risk for autism spectrum disorders.
CaMK4-dependent activation of AKT (show AKT1 Antibodies)/mTOR (show FRAP1 Antibodies) and CREM (show CREM Antibodies)-alpha underlies autoimmunity-associated Th17 imbalance.
CaMK4 regulates beta-cell proliferation and apoptosis in a CREB (show CREB1 Antibodies)-dependent manner and CaMK4-induced IRS-2 (show IRS2 Antibodies) expression is important in these processes
study suggests that the mutations in CAMK4 may lead to abnormal semen parameters
Phosphorylated Notch1 (show NOTCH1 Antibodies)-IC by CaMKIV increases Notch1 (show NOTCH1 Antibodies)-IC stability, which enhances osteoclast differentiation.
Pharmacological inhibition of CaMK4 recapitulated the observed defects in Cryptococcus neoformans phagocytosis. Furthermore, mice deficient in CaMK4 showed increased survival compared to wild-type mice upon infection with Cryptococcus neoformans. This increase in survival correlated with decreased expression of pattern recognition receptors on host phagocytes known to recognize Cryptococcus neoformans.
results imply that CaMKIV plays a role in maintenance the structure of chromatoid body by regulating the associations of proteins in it
CaMK4 activity is increased in T cells from systemic lupus erythematosus mice compared with the control group.
Results demonstrated that genetically inhibiting the CaMKK (show CAMKK2 Antibodies) pathway via CaMKKbeta or CaMK IV is detrimental in the response of female mice to cerebral ischemia
CaMKIV-mTOR (show FRAP1 Antibodies)-dependent autophagy is conserved in both immune and nonimmune/parenchymal cells and is fundamental for the respective functional and adaptive responses to septic insult.
The stimulation of CaMKII (show CAMK2G Antibodies) activity in the hippocampus is essential for rivastigmine-induced memory improvement in olfactory bulbectomized mice.
CaMKK (show CAMKK2 Antibodies)/CaMK IV pathway is a key endogenous protective mechanism in cerebral ischemia.
CaMKIV has opposing roles in nicotine and cocaine reward.
We identified the zebrafish homologue of CaMKIV (zCaMKIV) on the basis of biochemical characterization. zCaMKIV showed similar biochemical properties as well as tissue and subcellular distributions to rat CaMKIV (rCaMKIV)
Data suggest that Tyr (show TYR Antibodies)(99) phosphorylated calmodulin, as compared to non-phosphorylated, binds with a higher affinity at the calmodulin binding site (rich in basic amino acids) of CaM kinase IV leading to increased activation of CaM kinase IV.
conclude that the hypoxia-induced increased activation of CaM kinase IV cascade increases with the increase in the degree of cerebral tissue hypoxia as measured by cerebral tissue high energy phosphates in a curvilinear manner
The product of this gene belongs to the serine/threonine protein kinase family, and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. This enzyme is a multifunctional serine/threonine protein kinase with limited tissue distribution, that has been implicated in transcriptional regulation in lymphocytes, neurons and male germ cells.
calcium/calmodulin-dependent protein kinase type IV-like
, calcium/calmodulin-dependent protein kinase IV
, CAM kinase IV
, CAM kinase- GR
, brain Ca(2+)-calmodulin-dependent protein kinase type IV
, brain Ca++-calmodulin-dependent protein kinase type IV
, caM kinase-GR
, calcium/calmodulin-dependent protein kinase type IV
, calcium/calmodulin-dependent protein kinase type IV catalytic chain
, CAM kinase-GR
, Ca2+/calmodulin-dependent protein kinase type IV/Gr
, caMK IV
, Calmodulin-dependent protein kinase IV