Browse our PRKAG2 Proteins (PRKAG2)

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 Proteins) 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. PRKAG2-mutated iPSC-CMs (show Cd2ap Proteins) displayed functional and structural abnormalities, which were abolished by correcting the mutation in the patient's iPSCs using CRISPR technology.

2. gamma2 AMPK (show PRKAA1 Proteins) activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarcolemmal hyperpolarization-activated current (I f) and ryanodine receptor (show RYR3 Proteins)-derived diastolic local subsarcolemmal Ca(2 (show CA2 Proteins)+) release. In contrast, loss of gamma2 AMPK (show PRKAA1 Proteins) induces a reciprocal phenotype of increased heart rate, and prevents the adaptive intrinsic bradycardia of endurance training.

3. Case Report: PRKAG2 missense mutation causing glycogen (show GYS1 Proteins) storage disease and severe biventricular hypertrophy and high-grade atrio-ventricular block.

4. We highlight the potential for patients with PRKAG2 mutations.

5. 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.

6. 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.

7. 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.

8. 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.

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

10. 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).

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

1. gamma2 AMPK (show PRKAA1 Proteins) activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarcolemmal hyperpolarization-activated current (I f) and ryanodine receptor (show RYR3 Proteins)-derived diastolic local subsarcolemmal Ca(2 (show CA2 Proteins)+) release. In contrast, loss of gamma2 AMPK (show PRKAA1 Proteins) induces a reciprocal phenotype of increased heart rate, and prevents the adaptive intrinsic bradycardia of endurance training.

2. 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).

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

4. 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.

5. 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.

6. 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.

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

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

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

10. 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.