Ras-dependent pathways induce obstructive hypertrophy in echo-selected transgenic mice

Proceedings of the National Academy of Sciences of the United States of America

Volumn 94, Issue 9, 1997, Pages 4710-4715

  Gottshall, Kim R ^a,b   Hunter, John J ^a,b   Tanaka, Nobuaki ^a   Dalton, Nancy ^a   Becker, K David ^a,b   Ross Jr , John ^a   Chien, Kenneth R ^a,b  

^a UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

gene expression; hypertrophic cardiomyopathy; molecular signaling; regulation

Indexed keywords

MUTANT PROTEIN; MYOSIN LIGHT CHAIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; GENE EXPRESSION; HEART VENTRICLE OVERLOAD; HEART VENTRICLE PRESSURE; HYPERTROPHIC CARDIOMYOPATHY; MOUSE; NONHUMAN; ONCOGENE RAS; PHENOTYPE; PRIORITY JOURNAL; SARCOMERE; TRANSGENIC MOUSE;

AGE FACTORS; ANIMALS; ATRIAL NATRIURETIC FACTOR; FIBROSIS; GENE EXPRESSION; HEMODYNAMIC PROCESSES; HYPERTROPHY, LEFT VENTRICULAR; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MYOCARDIUM; MYOSIN LIGHT CHAINS; NATRIURETIC PEPTIDE, BRAIN; NERVE TISSUE PROTEINS; PHENOTYPE; RAS PROTEINS; RECOMBINANT FUSION PROTEINS; SELECTION (GENETICS); SIGNAL TRANSDUCTION; VARIATION (GENETICS);

EID: 0030989064     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.94.9.4710     Document Type: Article

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