A signaling role for dystrophin: inhibiting skeletal muscle atrophy pathways.
Skeletal muscle atrophy is a common comorbidity of cancer. The cellular signaling mechanisms that regulate muscle size constitute a balance of the protein breakdown pathways upregulated during atrophy, and the protein synthesis pathways that are activated during skeletal muscle hypertrophy. In this issue of Cancer Cell, Acharyya et al. demonstrate a new and surprising regulatory axis that is centered around dystrophin, the protein that is mutated in settings of muscular dystrophy. These data reposition dystrophin as a signaling protein and connect an important cellular complex required for the structural integrity of muscle to the pathways that modulate muscle size.
Glass
David J
DJ
Novartis Institutes for Biomedical Research, 400 Technology Square, Cambridge, Massachusetts 02139, USA. david.glass@novartis.com
D000818:Animals; D002100:Cachexia / Q000150:complications; D016189:Dystrophin / Q000378:metabolism / Q000502:physiology*; D049029:Dystrophin-Associated Proteins / Q000378:metabolism* / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D018482:Muscle, Skeletal / Q000378:metabolism; D009133:Muscular Atrophy / Q000150:complications / Q000378:metabolism*; D009369:Neoplasms / Q000150:complications* / Q000503:physiopathology; D015398:Signal Transduction
D016189:Dystrophin; D049029:Dystrophin-Associated Proteins