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Transgenic mice overexpressing mutant PRKAG2 define the cause of Wolff-Parkinson-White syndrome in glycogen storage cardiomyopathy.
N488I mutation of the gamma2-subunit results in bidirectional changes in AMP-activated protein kinase activity.
Increased glycogen stores due to gamma-AMPK overexpression protects against ischemia and reperfusion damage.
Glycogen storage diseases presenting as hypertrophic cardiomyopathy.
Aberrant activation of AMP-activated protein kinase remodels metabolic network in favor of cardiac glycogen storage.
Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy.
The genetic basis for cardiac remodeling.
Clinical outcome and phenotypic expression in LAMP2 cardiomyopathy.
Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations.
Glycogen Storage Disease
Glycogen Storage Disease Type IIb
Glycogen Storage Disease Type II
Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.