Journal article
Absence of caspase-3 protects against denervation-induced skeletal muscle atrophy
Abstract
The ubiquitin-proteasome system is a key proteolytic pathway activated during skeletal muscle atrophy. The proteasome, however, cannot degrade intact myofibrils or actinomyosin complexes. In rodent models of diabetes mellitus and uremia, caspase-3 is involved in actinomyosin cleavage, generating fragments that subsequently undergo ubiquitin-proteasome-mediated degradation. Here, we demonstrate that caspase-3 also mediates denervation-induced …
Authors
Plant PJ; Bain JR; Correa JE; Woo M; Batt J
Journal
Journal of Applied Physiology, Vol. 107, No. 1, pp. 224–234
Publisher
American Physiological Society
Publication Date
7 2009
DOI
10.1152/japplphysiol.90932.2008
ISSN
8750-7587
Associated Experts
Fields of Research (FoR)
Medical Subject Headings (MeSH)
AnimalsApoptosisCaspase 3Disease Models, AnimalGene Expression Regulation, EnzymologicMiceMice, Inbred C57BLMice, KnockoutMuscle DenervationMuscle ProteinsMuscle, SkeletalMuscular AtrophyPoly(ADP-ribose) PolymerasesProteasome Endopeptidase ComplexSKP Cullin F-Box Protein LigasesSignal TransductionTripartite Motif ProteinsUbiquitin-Protein Ligases