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机构地区:[1]遵义医学院人体解剖学教研室,遵义563003
出 处:《四川解剖学杂志》2012年第3期33-36,60,共5页Sichuan Journal of Anatomy
摘 要:骨骼肌萎缩是多种疾病的并发症之一,其机制可归因于蛋白质降解增加与合成受阻。近年来,人们发现蛋白质降解增加与肌肉环状指基因1(MuRF1)和肌肉萎缩盒F基因(MAFbx,atrogin-1)的表达增加有关。本文就这两个基因的研究进展作一综述。Skeletal muscle atrophy occurs in many chronic diseases and disuse conditions.Decreases in protein synthesis and increases in protein degradation both have been shown to contribute to muscle protein loss due to disuse,and recent work has delineated elements of both synthetic and proteolytic processes underlying muscle atrophy.The discovery of two muscle-specific E3 ubiquitin ligases,MAFbx/atrogin-1 and Muscle RING Finger-1(MuRF1),promoted an expectation of these molecules as targets for therapeutic development.The purpose of this review is to synthesize our current understanding of the two genes about molecular regulation of muscle atrophy.
分 类 号:R746.4[医药卫生—神经病学与精神病学]
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