The structure, function, and turnover of cardiac myosin in normal and myopathic Syrian hamsters.
Cardiac myosin was examined during the four pathologic stages of cardiomyopathy in strain BIO 14.6 of Syrian hamsters. It was determined that the Ca2+- and K+-ethylenediaminetetraacetic acid (EDTA)-activated ATPase activities of ventricular myosin were significantly reduced during the final stage of the inherited disease. One- and 2-dimensional gel electrophoresis of myosin samples at all stages failed to yield any evidence for a change in the subunit structure of myosin based on light chain number, molecular weight, and per cent composition. The final stage of the disease was characterized by altered protein metabolism. The rates of synthesis and degradation were both altered in the diseased tissue, and a net loss of myosin resulting from a substantial increase in the rate of degradation.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D009202:Cardiomyopathies / Q000378:metabolism*; D006224:Cricetinae; D004591:Electrophoresis, Polyacrylamide Gel; D005110:Extracellular Space / Q000378:metabolism; D007553:Isotope Labeling; D007700:Kinetics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D010649:Phenylalanine / Q000097:blood / Q000378:metabolism
D010649:Phenylalanine; D000251:Adenosine Triphosphatases; D009218:Myosins