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the PRKAG2 gene can be used for marker-assisted selection to improve the body measurement and meat quality traits in the Qinchuan cattle population.
No differences in PRKAG2 transcript abundance were detected in small intestine, liver or muscle. Correlation between gene expression level of PRKAG2 in rumen and average daily feed intake was detected in both seasons but the direction differed by season.
Alleles of 2 equine AMPK (show PRKAA1 Proteins) gamma subunit genes had no causative role in polysaccharide storage myopathy in horses
This study of patients with PRKAG2 mutations provides a more comprehensive view of the natural history of this disease and demonstrates a high risk of cardiac complications. Early recognition of this disease appears important to allow an appropriate management.
A novel missense genetic variant of unknown significance (GVUS) was detected in the PRKAG2 gene (c.869A>T, p.K290I). This novel GVUS has not been identified in any global population databases.
As in patients with PRKAG2 cardiomyopathy, iPS (show SLC27A4 Proteins) cell and mouse models are protected from cardiac fibrosis, and we define a crosstalk between AMPK (show PRKAA1 Proteins) and post-transcriptional regulation of TGFbeta (show TGFB1 Proteins) isoform signaling that has implications in fibrotic forms of cardiomyopathy.
Identify a novel, de novo PRKAG2 mutation (K475E) in the cystathionine beta-synthase (show CBS Proteins) 3 repeat, a region critical for AMP (show APRT Proteins) binding, which affects AMP-activated protein kinase (show PRKAA2 Proteins) activity, activates cell growth pathways, and results in cardiac hypertrophy, which can be reversed with rapamycin.
PRKAG2 polymorphism maybe important factor treating hypertensive patients with hydrochlorothiazide.
Data suggest different gamma-isoforms in AMPK (show PRKAA1 Proteins) can have different effects on enzyme activation; here, activation of AMPK (show PRKAA1 Proteins) by compound 991 is greater if AMPK (show PRKAA1 Proteins) contains PRKAG2 versus PRKAG1 (show PRKAG1 Proteins) or PRKAG3 (show PRKAG3 Proteins).
mice with chronic AMPK (show PRKAA1 Proteins) activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin (show GHRL Proteins) signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin (show INS Proteins) secretion. Humans bearing the homologous mutation manifest a congruent phenotype.
PRKAG2 cardiac syndrome may present with eccentric distribution of LVH, involving focal mid-infero-lateral pattern in the early disease stage, and more diffuse pattern but focusing on interventricular septum in advanced cases.
Overexpression of G100S mutation in PRKAG2 causes Wolff-Parkinson-White syndrome in transgenic zebrafish.
Its mutation causes AMPK (show PRKAA1 Proteins) signaling abnormality which leads to cardiac syndrome.
gamma2-specific AMPK (show PRKAA1 Proteins) activity was elevated in neonatal FNIP1-deficient myocardium, supporting a role for FNIP1 as a negative regulator of AMPK (show PRKAA1 Proteins).
Increased AMPK-gamma2 activation is required to protect against myocardial ischemia/reperfusion injury.
These results demonstrate that expression of AMPK subunit gamma-2(NI) and AMPK subunit gamma-2(RG) mutations at physiological levels can induce beneficial metabolic effects but that this is accompanied by Wolff-Parkinson-White Syndrome syndrome.
Prkag2 point mutation causes glycogen (show GYS1 Proteins) storage via enhanced insulin (show INS Proteins) sensitivity and AKT (show AKT1 Proteins) activation. It stimulates postnatal cardiomyocyte proliferation by downregulating FoxO (show FOXO3 Proteins). It promotes cardiac hypertrophy via mTOR (show FRAP1 Proteins) activation in developed hearts.
We have demonstrated that a third AMPK gamma2 variant, gamma2-3B, is increasingly expressed in the developing heart.
important for cigarette smoking-induced IL-8 (show IL8 Proteins) production by lung epithelial cells
CNTF (show CNTF Proteins)(Ax15) bypasses diet-induced leptin (show LEP Proteins) resistance to reduce hypothalamic AMPK (show PRKAA1 Proteins) activity
CR resulted in incerasd AMPK (show PRKAA1 Proteins) phosphorylation and, hence, activation. GHR (show GHR Proteins) knockout animals also exhibited invrease p-AMPK (show PRKAA1 Proteins) levels. P-AMPK (show PRKAA1 Proteins) levels were not altered by disruption of the GHR (show GHR Proteins) gene.
Despite high glycogen (show GYS1 Proteins) content, the TGT400N heart is not protected against ischemia-reperfusion injury.
AMP-activated protein kinase (AMPK) is a heterotrimeric protein composed of a catalytic alpha subunit, a noncatalytic beta subunit, and a noncatalytic regulatory gamma subunit. Various forms of each of these subunits exist, encoded by different genes. AMPK is an important energy-sensing enzyme that monitors cellular energy status and functions by inactivating key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. This gene is a member of the AMPK gamma subunit family and encodes a protein with four cystathionine beta-synthase domains. Mutations in this gene have been associated with ventricular pre-excitation (Wolff-Parkinson-White syndrome), progressive conduction system disease and cardiac hypertrophy. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
5'-AMP-activated protein kinase subunit gamma-2
, AMP-activated protein kinase gamma2 subunit
, AMPK gamma 2
, adenosine monophosphate-activated protein kinase gamma 2-subunit
, 5'-AMP-activated protein kinase gamma-2 non-catalytic subunit
, protein kinase, AMP-activated, gamma 2 non-catalytic subunit
, AMPK-activated protein kinase gamma-2 subunit
, AMPK subunit gamma-2
, 5-AMP-activated protein kinase, gamma-2 subunit
, AMPK gamma-2 chain
, AMPK gamma2