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anti-Human PRKAA2 Antibodies:
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Cow (Bovine) Polyclonal PRKAA2 Primary Antibody for 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
Show all 3 Pubmed References
Human Polyclonal PRKAA2 Primary Antibody for 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 for 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 for 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 (show PRKAA1 Antibodies)-ULK1 (show ULK1 Antibodies) signaling dysregulation independently of HIF-1A (show HIF1A Antibodies).
PRKAA deletion promoted mitochondrial fragmentation in vascular endothelial cells by inhibiting the autophagy-dependent degradation of DNM1L (show DNM1L Antibodies).
AMPK phosphorylates DNMT1, RBBP7, and HAT1 and increases interactions of DNMT1, RBBP7, and HAT1.
PGC-1alpha protein was higher after HIHVT than after SIT (p < 0.05). Moreover, the AMPKpTHR172/AMPK (show PRKAA1 Antibodies) ratio increased at post after SIT (p < 0.05), whereas this effect was delayed after HIHVT as it increased after 3 h
TNF-alpha (show TNF Antibodies) treatment of colonic rho(0) cells augmented IL-8 (show IL8 Antibodies) expression by 9-fold (P < 0.01) via NF-kappaB (show NFKB1 Antibodies) compared to TNF-alpha (show TNF Antibodies)-treated control. Moreover, reduced mitochondrial function facilitated TNF-alpha (show TNF Antibodies)-mediated NF-kappaB (show NFKB1 Antibodies) luciferase promoter activity as a result of lowered inhibitory IkappaBalpha (show NFKBIA Antibodies) (nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor, alpha), leading to elevated NF-kappaB (show NFKB1 Antibodies). ...
Results highlight the contribution of AMPKalpha2 as a mechanism for controlling bladder cancer growth by regulating proliferation through mTOR (show FRAP1 Antibodies) suppression and induction of p27 (show PAK2 Antibodies) protein levels, thus indicating how AMPKalpha2 loss may contribute to tumorigenesis.
AMPK (show PRKAA1 Antibodies) phosphorylation of cortactin (show CTTN Antibodies) followed by SIRT1 (show SIRT1 Antibodies) deacetylation modulates the interaction of cortactin (show CTTN Antibodies) and cortical-actin in response to shear stress. Functionally, this AMPK (show PRKAA1 Antibodies)/SIRT1 (show SIRT1 Antibodies) coregulated cortactin (show CTTN Antibodies)-F-actin dynamics is required for endothelial nitric oxide synthase (show NOS3 Antibodies) subcellular translocation/activation and is atheroprotective.
Data suggest that the AMPK (show PRKAA1 Antibodies)-TBC1D4 (show TBC1D4 Antibodies) signaling axis is likely mediating the improved muscle insulin (show INS Antibodies) sensitivity after contraction/exercise and illuminates an important and physiologically relevant role of AMPK (show PRKAA1 Antibodies) in skeletal muscle.
inactivation of AMPKalpha2, but not AMPKalpha1 (show PRKAA1 Antibodies), abrogates the tumor attenuation caused by UBE2O (show UBE2O Antibodies) loss.
Our findings demonstrate that the AMPKalpha2 catalytic subunit in Kiss1 (show KISS1 Antibodies) cells is dispensable for body weight and reproductive function in mice but is necessary for the reproductive adaptations to conditions of acute metabolic distress.
AMPKalpha2 activation prevents cardiac hypertrophy predominantly by inhibiting O-GlcNAcylation.
Ampk (show PRKAA1 Antibodies) is required for exercise-induced mitophagy in muscle.
This novel mechanism explains how CDK4 (show CDK4 Antibodies) promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK (show PRKAA1 Antibodies).
High AMPKalpha2 phosphorylation is associated with abdominal aortic aneurysm.
Rac1 and AMPK (show PRKAA1 Antibodies) together account for almost the entire ex vivo contraction response in muscle glucose transport, whereas only Rac1, but not alpha2 AMPK (show PRKAA1 Antibodies), 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 (show PRKAA1 Antibodies) we achieved reduced renal AMPK (show PRKAA1 Antibodies) activity, accompanied by a shift to a moderate water- and salt-wasting phenotype. Thus we confirm the physiologically relevant role of AMPK (show PRKAA1 Antibodies) in the kidney.
Findings show that decreased AMPK (show PRKAA1 Antibodies) 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 (show PRKAA1 Antibodies) muscle deficient mice is most likely unrelated to regulation of brain dopamine content and metabolism.
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 (show PRKAA1 Antibodies) activator AICAR (show ATIC Antibodies) is inhibitory to nuclear maturation in bovine oocytes due to activation of AMPK (show PRKAA1 Antibodies) [AMP-activated protein kinase alpha (show PAK1 Antibodies) 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