MacLennan P A, Edwards R H
Department of Medicine, University of Liverpool, U.K.
Biochem J. 1990 Jun 15;268(3):795-7. doi: 10.1042/bj2680795.
mdx mice lack the protein dystrophin, the absence of which causes Duchenne muscular dystrophy in humans. To examine how mdx mice maintain muscle mass despite dystrophin deficiency, we measured protein turnover rates in muscles of mdx and wild-type (C57BL/10) mice in vivo. At all ages studied, rates of muscle protein synthesis and degradation were higher in mdx than in C57BL/10 mice.
mdx小鼠缺乏抗肌萎缩蛋白,该蛋白的缺失会导致人类患杜兴氏肌肉营养不良症。为了研究mdx小鼠在缺乏抗肌萎缩蛋白的情况下是如何维持肌肉质量的,我们在体内测量了mdx小鼠和野生型(C57BL/10)小鼠肌肉中的蛋白质周转率。在所有研究的年龄段中,mdx小鼠的肌肉蛋白质合成和降解率均高于C57BL/10小鼠。