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Co-immunoprecipitation and binding assay data from both cell types show that the H1/A (but not H2/B) isoform of NDPK is associated with AMPK (show PRKAA1 ELISA Kits) complexes containing the alpha1 (but not alpha2) catalytic subunit.
AMPK phosphorylates DNMT1, RBBP7, and HAT1 and increases interactions of DNMT1, RBBP7, and HAT1.
PGC-1alpha (show PPARGC1A ELISA Kits) protein was higher after HIHVT than after SIT (p < 0.05). Moreover, the AMPKpTHR172/AMPK (show PRKAA1 ELISA Kits) 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 ELISA Kits) treatment of colonic rho(0) cells augmented IL-8 (show IL8 ELISA Kits) expression by 9-fold (P < 0.01) via NF-kappaB (show NFKB1 ELISA Kits) compared to TNF-alpha (show TNF ELISA Kits)-treated control. Moreover, reduced mitochondrial function facilitated TNF-alpha (show TNF ELISA Kits)-mediated NF-kappaB (show NFKB1 ELISA Kits) luciferase promoter activity as a result of lowered inhibitory IkappaBalpha (show NFKBIA ELISA Kits) (nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor, alpha), leading to elevated NF-kappaB (show NFKB1 ELISA Kits). ...
Results highlight the contribution of AMPKalpha2 as a mechanism for controlling bladder cancer growth by regulating proliferation through mTOR (show FRAP1 ELISA Kits) suppression and induction of p27 (show PAK2 ELISA Kits) protein levels, thus indicating how AMPKalpha2 loss may contribute to tumorigenesis.
AMPK (show PRKAA1 ELISA Kits) phosphorylation of cortactin (show CTTN ELISA Kits) followed by SIRT1 (show SIRT1 ELISA Kits) deacetylation modulates the interaction of cortactin (show CTTN ELISA Kits) and cortical-actin in response to shear stress. Functionally, this AMPK (show PRKAA1 ELISA Kits)/SIRT1 (show SIRT1 ELISA Kits) coregulated cortactin (show CTTN ELISA Kits)-F-actin dynamics is required for endothelial nitric oxide synthase (show NOS3 ELISA Kits) subcellular translocation/activation and is atheroprotective.
Data suggest that the AMPK (show PRKAA1 ELISA Kits)-TBC1D4 signaling axis is likely mediating the improved muscle insulin (show INS ELISA Kits) sensitivity after contraction/exercise and illuminates an important and physiologically relevant role of AMPK (show PRKAA1 ELISA Kits) in skeletal muscle.
inactivation of AMPKalpha2, but not AMPKalpha1, abrogates the tumor attenuation caused by UBE2O loss.
Our findings demonstrate that the AMPKalpha2 catalytic subunit in Kiss1 (show KISS1 ELISA Kits) cells is dispensable for body weight and reproductive function in mice but is necessary for the reproductive adaptations to conditions of acute metabolic distress.
Binding of miR (show MLXIP ELISA Kits)-27a to the 3'-UTR (show UTS2R ELISA Kits) of the AMPKalpha2 gene was required to increase the sensitivity of breast cancer cells to metformin.
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 ELISA Kits) activator AICAR (show ATIC ELISA Kits) is inhibitory to nuclear maturation in bovine oocytes due to activation of AMPK (show PRKAA1 ELISA Kits) [AMP-activated protein kinase alpha (show PAK1 ELISA Kits) 1 subunit].
these results elucidate an oncogenic role for UBE2O in promoting mTOR (show FRAP1 ELISA Kits)-HIF1a (show HIF1A ELISA Kits) signaling, and suggest that therapeutic targeting of UBE2O may restore AMPKa2 to suppress tumorigenesis.
This novel mechanism explains how CDK4 (show CDK4 ELISA Kits) promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK (show PRKAA1 ELISA Kits).
High AMPKalpha2 phosphorylation is associated with abdominal aortic aneurysm.
Rac1 and AMPK (show PRKAA1 ELISA Kits) together account for almost the entire ex vivo contraction response in muscle glucose transport, whereas only Rac1, but not alpha2 AMPK (show PRKAA1 ELISA Kits), 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 ELISA Kits) we achieved reduced renal AMPK (show PRKAA1 ELISA Kits) activity, accompanied by a shift to a moderate water- and salt-wasting phenotype. Thus we confirm the physiologically relevant role of AMPK (show PRKAA1 ELISA Kits) in the kidney.
Findings show that decreased AMPK (show PRKAA1 ELISA Kits) 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 ELISA Kits) muscle deficient mice is most likely unrelated to regulation of brain dopamine content and metabolism.
Hypoxia reduces HNF4alpha/MODY1 (show HNF4A ELISA Kits) protein expression in pancreatic beta-cells by activating AMP-activated protein kinase.
These studies reveal a novel mechanism in which CYP2J2 (show CYP2J2 ELISA Kits) and epoxyeicosatrienoic acids enhanced Akt1 (show AKT1 ELISA Kits) 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.
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