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anti-Human PRKAA2 Antikörper:
anti-Rat (Rattus) PRKAA2 Antikörper:
anti-Mouse (Murine) PRKAA2 Antikörper:
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Cow (Bovine) Polyclonal PRKAA2 Primary Antibody für WB - ABIN151705
Rubin, Magliola, Feng, Jones, Hale: Metabolic activation of AMP kinase in vascular smooth muscle. in Journal of applied physiology (Bethesda, Md. : 1985) 2004
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Human Polyclonal PRKAA2 Primary Antibody für IF (p), IHC (p) - ABIN680458
Fu, Zhu, Dodson, Du: AMP-activated protein kinase stimulates Warburg-like glycolysis and activation of satellite cells during muscle regeneration. in The Journal of biological chemistry 2015
Show all 2 Pubmed References
Cow (Bovine) Polyclonal PRKAA2 Primary Antibody für IP - ABIN153316
Gusarova, Dada, Kelly, Brodie, Witters, Chandel, Sznajder: Alpha1-AMP-activated protein kinase regulates hypoxia-induced Na,K-ATPase endocytosis via direct phosphorylation of protein kinase C zeta. in Molecular and cellular biology 2009
Human Polyclonal PRKAA2 Primary Antibody für ELISA, EIA - ABIN4280438
Dong, Zhang, Liang, Xie, Zhao, Asfa, Choi, Zou: Reduction of AMP-activated protein kinase alpha2 increases endoplasmic reticulum stress and atherosclerosis in vivo. in Circulation 2010
Lack of mitochondrial DNA impairs chemical hypoxia-induced autophagy in liver tumor cells through reactive oxygen species-AMPK (zeige PRKAA1 Antikörper)-ULK1 (zeige ULK1 Antikörper) signaling dysregulation independently of HIF-1A (zeige HIF1A Antikörper).
PRKAA deletion promoted mitochondrial fragmentation in vascular endothelial cells by inhibiting the autophagy-dependent degradation of DNM1L (zeige DNM1L Antikörper).
AMPK phosphorylates DNMT1, RBBP7, and HAT1 and increases interactions of DNMT1, RBBP7, and HAT1.
PGC-1alpha (zeige PPARGC1A Antikörper) protein was higher after HIHVT than after SIT (p < 0.05). Moreover, the AMPKpTHR172/AMPK (zeige PRKAA1 Antikörper) ratio increased at post after SIT (p < 0.05), whereas this effect was delayed after HIHVT as it increased after 3 h
TNF-alpha (zeige TNF Antikörper) treatment of colonic rho(0) cells augmented IL-8 (zeige IL8 Antikörper) expression by 9-fold (P < 0.01) via NF-kappaB (zeige NFKB1 Antikörper) compared to TNF-alpha (zeige TNF Antikörper)-treated control. Moreover, reduced mitochondrial function facilitated TNF-alpha (zeige TNF Antikörper)-mediated NF-kappaB (zeige NFKB1 Antikörper) luciferase promoter activity as a result of lowered inhibitory IkappaBalpha (zeige NFKBIA Antikörper) (nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor, alpha), leading to elevated NF-kappaB (zeige NFKB1 Antikörper). ...
Results highlight the contribution of AMPKalpha2 as a mechanism for controlling bladder cancer growth by regulating proliferation through mTOR (zeige FRAP1 Antikörper) suppression and induction of p27 (zeige PAK2 Antikörper) protein levels, thus indicating how AMPKalpha2 loss may contribute to tumorigenesis.
AMPK (zeige PRKAA1 Antikörper) phosphorylation of cortactin (zeige CTTN Antikörper) followed by SIRT1 (zeige SIRT1 Antikörper) deacetylation modulates the interaction of cortactin (zeige CTTN Antikörper) and cortical-actin in response to shear stress. Functionally, this AMPK (zeige PRKAA1 Antikörper)/SIRT1 (zeige SIRT1 Antikörper) coregulated cortactin (zeige CTTN Antikörper)-F-actin dynamics is required for endothelial nitric oxide synthase (zeige NOS3 Antikörper) subcellular translocation/activation and is atheroprotective.
Data suggest that the AMPK (zeige PRKAA1 Antikörper)-TBC1D4 (zeige TBC1D4 Antikörper) signaling axis is likely mediating the improved muscle insulin (zeige INS Antikörper) sensitivity after contraction/exercise and illuminates an important and physiologically relevant role of AMPK (zeige PRKAA1 Antikörper) in skeletal muscle.
inactivation of AMPKalpha2, but not AMPKalpha1 (zeige PRKAA1 Antikörper), abrogates the tumor attenuation caused by UBE2O (zeige UBE2O Antikörper) loss.
Our findings demonstrate that the AMPKalpha2 catalytic subunit in Kiss1 (zeige KISS1 Antikörper) cells is dispensable for body weight and reproductive function in mice but is necessary for the reproductive adaptations to conditions of acute metabolic distress.
This novel mechanism explains how CDK4 (zeige CDK4 Antikörper) promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK (zeige PRKAA1 Antikörper).
High AMPKalpha2 phosphorylation is associated with abdominal aortic aneurysm.
Rac1 and AMPK (zeige PRKAA1 Antikörper) together account for almost the entire ex vivo contraction response in muscle glucose transport, whereas only Rac1, but not alpha2 AMPK (zeige PRKAA1 Antikörper), regulates muscle glucose uptake during submaximal exercise in vivo.
we used the Cre-loxP system to knock down AMPKalpha2 expression in renal epithelial cells. Combining this approach with the systemic deletion of AMPKalpha1 (zeige PRKAA1 Antikörper) we achieved reduced renal AMPK (zeige PRKAA1 Antikörper) activity, accompanied by a shift to a moderate water- and salt-wasting phenotype. Thus we confirm the physiologically relevant role of AMPK (zeige PRKAA1 Antikörper) in the kidney.
Findings show that decreased AMPK (zeige PRKAA1 Antikörper) activity in muscle leads to decreased voluntary activity which is not due to secondary abnormalities in dopamine levels in the ventral striatum or sensitivity to cocaine. Thus, decreased voluntary activity in AMPK (zeige PRKAA1 Antikörper) muscle deficient mice is most likely unrelated to regulation of brain dopamine content and metabolism.
Hypoxia reduces HNF4alpha/MODY1 (zeige HNF4A Antikörper) protein expression in pancreatic beta-cells by activating AMP-activated protein kinase.
These studies reveal a novel mechanism in which CYP2J2 (zeige CYP2J2 Antikörper) and epoxyeicosatrienoic acids enhanced Akt1 (zeige AKT1 Antikörper) nuclear translocation through interaction with AMPKalpha2beta2gamma1 and protect against cardiac hypertrophy.
Single SNP and haplotype analyses revealed weak associations between the PRKAA2 genotypes and loin muscle area in the investigated populations.
Endometrial inflammatory responses to lipopolysaccharide were also reduced by small molecules that activate or inhibit the intracellular sensor of energy, AMP-activated protein kinase (AMPK).
The investigation of PRKAA2 genetic polymorphisms in three Chinese indigenous bovine breeds [Qinchuan (n = 328), Nanyang (n = 278), Jiaxian (n = 148)] and yak (n = 57), is reported.
These data show that the AMPK (zeige PRKAA1 Antikörper) activator AICAR (zeige ATIC Antikörper) is inhibitory to nuclear maturation in bovine oocytes due to activation of AMPK (zeige PRKAA1 Antikörper) [AMP-activated protein kinase alpha (zeige PAK1 Antikörper) 1 subunit].
The protein encoded by this gene is a catalytic subunit of the AMP-activated protein kinase (AMPK). AMPK is a heterotrimer consisting of an alpha catalytic subunit, and non-catalytic beta and gamma subunits. AMPK is an important energy-sensing enzyme that monitors cellular energy status. In response to cellular metabolic stresses, AMPK is activated, and thus phosphorylates and inactivates acetyl-CoA carboxylase (ACC) and beta-hydroxy beta-methylglutaryl-CoA reductase (HMGCR), key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. Studies of the mouse counterpart suggest that this catalytic subunit may control whole-body insulin sensitivity and is necessary for maintaining myocardial energy homeostasis during ischemia.
5'-AMP-activated protein kinase catalytic subunit alpha-2
, 5'-AMP-activated protein kinase, catalytic alpha-2 chain
, ACACA kinase
, AMPK subunit alpha-2
, AMPK-alpha-2 chain
, HMGCR kinase
, acetyl-CoA carboxylase kinase
, hydroxymethylglutaryl-CoA reductase kinase
, AMP-activated protein kinase
, AMPK alpha-2 chain
, AMP-activated protein kinase alpha-2 variant B
, AMP-activated protein kinase alpha 2
, protein kinase AMP-activated alpha 2 catalytic subunit
, SNF1-like protein AMPK
, 5'-AMP-activated protein kinase alpha-2 catalytic subunit
, AMP-activated protein kinase alpha 2 catalytic subunit
, protein kinase, AMP-activated, alpha 2 catalytic subunit
, AMPK-activated protein kinase alpha-2 subunit