Enhanced myosin function due to a point mutation causing a familial hypertrophic cardiomyopathy.
Moss
R L
RL
Department of Physiology, University of Wisconsin Medical School, Madison, WI, USA. rimoss@physiology.wisc.edu
Periera
J S
JS
D000199:Actins / Q000502:physiology; D019943:Amino Acid Substitution; D000818:Animals; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics*; D006801:Humans; D009218:Myosins / Q000235:genetics* / Q000502:physiology; D017354:Point Mutation
D000199:Actins; D009218:Myosins