anti-PRKAG2 (PRKAG2) Antikörper

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

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) Interaktionspartner

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

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

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 (zeige SLC27A4 Antikörper) cell and mouse models are protected from cardiac fibrosis, and we define a crosstalk between AMPK (zeige PRKAA1 Antikörper) and post-transcriptional regulation of TGFbeta (zeige TGFB1 Antikörper) isoform signaling that has implications in fibrotic forms of cardiomyopathy.

4. Identify a novel, de novo PRKAG2 mutation (K475E) in the cystathionine beta-synthase (zeige CBS Antikörper) 3 repeat, a region critical for AMP (zeige APRT Antikörper) binding, which affects AMP-activated protein kinase (zeige PRKAA2 Antikörper) 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 (zeige PRKAA1 Antikörper) can have different effects on enzyme activation; here, activation of AMPK (zeige PRKAA1 Antikörper) by compound 991 is greater if AMPK (zeige PRKAA1 Antikörper) contains PRKAG2 versus PRKAG1 (zeige PRKAG1 Antikörper) or PRKAG3 (zeige PRKAG3 Antikörper).

7. mice with chronic AMPK (zeige PRKAA1 Antikörper) activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin (zeige GHRL Antikörper) signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin (zeige INS Antikörper) 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 (zeige PRKAA1 Antikörper) signaling abnormality which leads to cardiac syndrome.

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

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

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

3. mice with chronic AMPK (zeige PRKAA1 Antikörper) activation, resulting from mutation of the AMPK gamma2 subunit, exhibit ghrelin (zeige GHRL Antikörper) signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin (zeige INS Antikörper) 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 (zeige GYS1 Antikörper) storage via enhanced insulin (zeige INS Antikörper) sensitivity and AKT (zeige AKT1 Antikörper) activation. It stimulates postnatal cardiomyocyte proliferation by downregulating FoxO (zeige FOXO3 Antikörper). It promotes cardiac hypertrophy via mTOR (zeige FRAP1 Antikörper) 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 (zeige IL8 Antikörper) production by lung epithelial cells

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

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

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