Browse our anti-PRKAG2 (PRKAG2) Antibodies

Cow (Bovine) Protein Kinase, AMP-Activated, gamma 2 Non-Catalytic Subunit (PRKAG2) interaction partners

1. the PRKAG2 gene can be used for marker-assisted selection to improve the body measurement and meat quality traits in the Qinchuan cattle population.

2. 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.

Horse (Equine) Protein Kinase, AMP-Activated, gamma 2 Non-Catalytic Subunit (PRKAG2) interaction partners

1. Alleles of 2 equine AMPK (show PRKAA1 Antibodies) gamma subunit genes had no causative role in polysaccharide storage myopathy in horses

Human Protein Kinase, AMP-Activated, gamma 2 Non-Catalytic Subunit (PRKAG2) interaction partners

1. 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.

2. 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.

3. As in patients with PRKAG2 cardiomyopathy, iPS (show SLC27A4 Antibodies) cell and mouse models are protected from cardiac fibrosis, and we define a crosstalk between AMPK (show PRKAA1 Antibodies) and post-transcriptional regulation of TGFbeta (show TGFB1 Antibodies) isoform signaling that has implications in fibrotic forms of cardiomyopathy.

4. Identify a novel, de novo PRKAG2 mutation (K475E) in the cystathionine beta-synthase (show CBS Antibodies) 3 repeat, a region critical for AMP (show APRT Antibodies) binding, which affects AMP-activated protein kinase (show PRKAA2 Antibodies) activity, activates cell growth pathways, and results in cardiac hypertrophy, which can be reversed with rapamycin.

5. PRKAG2 polymorphism maybe important factor treating hypertensive patients with hydrochlorothiazide.

6. Data suggest different gamma-isoforms in AMPK (show PRKAA1 Antibodies) can have different effects on enzyme activation; here, activation of AMPK (show PRKAA1 Antibodies) by compound 991 is greater if AMPK (show PRKAA1 Antibodies) contains PRKAG2 versus PRKAG1 (show PRKAG1 Antibodies) or PRKAG3 (show PRKAG3 Antibodies).

7. mice with chronic AMPK (show PRKAA1 Antibodies) activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin (show GHRL Antibodies) signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin (show INS Antibodies) secretion. Humans bearing the homologous mutation manifest a congruent phenotype.

8. 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.

9. Overexpression of G100S mutation in PRKAG2 causes Wolff-Parkinson-White syndrome in transgenic zebrafish.

10. Its mutation causes AMPK (show PRKAA1 Antibodies) signaling abnormality which leads to cardiac syndrome.

Mouse (Murine) Protein Kinase, AMP-Activated, gamma 2 Non-Catalytic Subunit (PRKAG2) interaction partners

1. gamma2-specific AMPK (show PRKAA1 Antibodies) activity was elevated in neonatal FNIP1 (show FNIP1 Antibodies)-deficient myocardium, supporting a role for FNIP1 (show FNIP1 Antibodies) as a negative regulator of AMPK (show PRKAA1 Antibodies).

2. Increased AMPK-gamma2 activation is required to protect against myocardial ischemia/reperfusion injury.

3. mice with chronic AMPK (show PRKAA1 Antibodies) activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin (show GHRL Antibodies) signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin (show INS Antibodies) secretion. Humans bearing the homologous mutation manifest a congruent phenotype.

4. 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.

5. Prkag2 point mutation causes glycogen (show GYS1 Antibodies) storage via enhanced insulin (show INS Antibodies) sensitivity and AKT (show AKT1 Antibodies) activation. It stimulates postnatal cardiomyocyte proliferation by downregulating FoxO (show FOXO3 Antibodies). It promotes cardiac hypertrophy via mTOR (show FRAP1 Antibodies) activation in developed hearts.

6. We have demonstrated that a third AMPK gamma2 variant, gamma2-3B, is increasingly expressed in the developing heart.

7. important for cigarette smoking-induced IL-8 (show IL8 Antibodies) production by lung epithelial cells

8. CNTF (show CNTF Antibodies)(Ax15) bypasses diet-induced leptin (show LEP Antibodies) resistance to reduce hypothalamic AMPK (show PRKAA1 Antibodies) activity

9. CR resulted in incerasd AMPK (show PRKAA1 Antibodies) phosphorylation and, hence, activation. GHR (show GHR Antibodies) knockout animals also exhibited invrease p-AMPK (show PRKAA1 Antibodies) levels. P-AMPK (show PRKAA1 Antibodies) levels were not altered by disruption of the GHR (show GHR Antibodies) gene.

10. Despite high glycogen (show GYS1 Antibodies) content, the TGT400N heart is not protected against ischemia-reperfusion injury.