Progressive loss of creatine maintains a near normal ΔG∼ATP in transgenic mouse hearts with cardiomyopathy caused by overexpressing Gsα

Journal of Molecular and Cellular Cardiology

Volumn 48, Issue 4, 2010, Pages 591-599

  Shen, Weiqun ^a,b   Vatner, Dorothy E ^c   Vatner, Stephen F ^c   Ingwall, Joanne S ^a  

^a BRIGHAM AND WOMEN S HOSPITAL   (United States)

^b EAST CHINA NORMAL UNIVERSITY   (China)

^c RUTGERS NEW JERSEY MEDICAL SCHOOL   (United States)

Author keywords

G ATP; Adenosine triphosphate; Cardiomyopathy; Creatine; Gs transgenic mice

Indexed keywords

ADENOSINE DIPHOSPHATE; ADENOSINE TRIPHOSPHATE; CREATINE; GUANINE NUCLEOTIDE BINDING PROTEIN ALPHA SUBUNIT;

AGE; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CARDIOMYOPATHY; CONTROLLED STUDY; HEART CONTRACTION; HEART FAILURE; HEART MUSCLE CONTRACTILITY; HEART MUSCLE METABOLISM; HEART WORK; HYDROLYSIS; ISOLATED HEART; LONGITUDINAL STUDY; MOUSE; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE; WILD TYPE;

ADENOSINE DIPHOSPHATE; ADENOSINE TRIPHOSPHATE; ANIMALS; CARDIOMEGALY; CARDIOMYOPATHIES; CREATINE; CYTOSOL; GTP-BINDING PROTEIN ALPHA SUBUNITS, GS; HYDROLYSIS; LINEAR MODELS; MAGNETIC RESONANCE SPECTROSCOPY; MICE; MICE, TRANSGENIC; MYOCARDIUM; PROTEIN ISOFORMS; RECEPTORS, ADRENERGIC, BETA;

MUS; MUS MUSCULUS;

EID: 77649274890     PISSN: 00222828     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2009.10.029     Document Type: Article

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