title: Sprinting without myostatin: a genetic determinant of athletic prowess.
abstract: Genetic studies in several species have demonstrated that myostatin (MSTN) normally functions to limit skeletal muscle mass. In a recent study, Mosher et al. reported that a mutation in the canine MSTN gene is responsible for the double-muscling phenotype seen in 'bully' whippets. Furthermore, they show that loss of even one functional MSTN allele seems to confer a competitive advantage to racing whippets, providing the first definitive evidence that loss of myostatin function can enhance athletic performance.
authors: Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, PCTB 803, 725 North Wolfe Street, Baltimore, MD 21205, USA. sjlee@jhmi.edu
authors: Se-Jin
authors: SJ
authors: Lee
mesh_terms: D000483:Alleles; D000818:Animals; D054874:Athletic Performance / Q000502:physiology*; D004285:Dogs; D006801:Humans; D051379:Mice; D018482:Muscle, Skeletal / Q000502:physiology; D009154:Mutation; D055435:Myostatin; D012756:Sheep; D016212:Transforming Growth Factor beta / Q000235:genetics* / Q000378:metabolism
chemical_list: C525911:MSTN protein, human; C525912:Mstn protein, mouse; D055435:Myostatin; D016212:Transforming Growth Factor beta