Loaded Shortening, Power Output, and Rate of Force Redevelopment Are Increased With Knockout of Cardiac Myosin Binding Protein-C

Circulation Research

Volumn 93, Issue 8, 2003, Pages 752-758

  Korte, F Steven ^a   McDonald, Kerry S ^a,c   Harris, Samantha P ^b   Moss, Richard L ^b  

^a University of Missouri   (United States)

^b UNIVERSITY OF WISCONSIN MADISON   (United States)

^c Univ of Missouri   (United States)

Author keywords

Cardiac contractility; Cardiac myocytes; Myosin binding protein C; Power output; Sarcomere proteins

Indexed keywords

CALCIUM; MYOSIN BINDING PROTEIN C; CARRIER PROTEIN; MYOSIN-BINDING PROTEIN C;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DISEASE ASSOCIATION; FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; FORCE TRANSDUCER; GENE MUTATION; HEART MUSCLE CONTRACTILE FORCE; HEART WORK; KNOCKOUT MOUSE; MOUSE; MUSCLE FORCE; MUSCLE ISOMETRIC CONTRACTION; MUSCLE STRENGTH; MYOFILAMENT; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN STRUCTURE; REGULATORY MECHANISM; SARCOMERE; WORK CAPACITY; ANIMAL; CELL CULTURE; CYTOLOGY; DRUG EFFECT; GENETICS; HEART CONTRACTION; HEART MUSCLE CELL; KINETICS; MOUSE MUTANT; PHYSIOLOGY;

ANIMALS; CALCIUM; CARRIER PROTEINS; CELLS, CULTURED; KINETICS; MICE; MICE, KNOCKOUT; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC;

EID: 0142024741     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.0000096363.85588.9A     Document Type: Article

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