萎缩
泛素
肌肉萎缩
肌发生
骨骼肌
生物
基因
泛素连接酶
细胞生物学
化学
遗传学
内分泌学
作者
Sue C. Bodine,Esther Latres,Susanne Baumhueter,Venus Lai,Lorna Nuñez,Brian Clarke,William Poueymirou,Frank J. Panaro,Erqian Na,Kumar Dharmarajan,Zhen‐Qiang Pan,David M. Valenzuela,Thomas M. DeChiara,Trevor N. Stitt,George D. Yancopoulos,David J. Glass
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2001-11-23
卷期号:294 (5547): 1704-1708
被引量:3309
标识
DOI:10.1126/science.1065874
摘要
Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 ( MuRF1 ), and a gene we designate Muscle Atrophy F-box ( MAFbx ), the latter being a member of the SCF family of E3 ubiquitin ligases. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.
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