PI3K/AKT/mTOR通路
RPTOR公司
骨骼肌
雷帕霉素的作用靶点
西罗莫司
细胞生物学
蛋白激酶B
激酶
磷酸化
mTORC2型
化学
生物
癌症研究
mTORC1型
信号转导
内分泌学
生物化学
作者
Craig A. Goodman,John W. Frey,Danielle Mabrey,Brittany L. Jacobs,Hannah C. Lincoln,Jae‐Sung You,Troy A. Hornberger
标识
DOI:10.1113/jphysiol.2011.218255
摘要
Non‐Technical Summary Chronic mechanical loading (CML) of skeletal muscle induces growth and this effect can be blocked by the drug rapamycin. Rapamycin is considered to be a highly specific inhibitor of the mammalian target of rapamycin (mTOR), and thus, many have concluded that mTOR plays a key role in CML‐induced growth. However, direct evidence that mTOR confers the CML‐induced activation of growth promoting events such as hypertrophy, hyperplasia and ribosome biogenesis is lacking. This study addressed that gap in knowledge by using a specialized line of transgenic mice. Surprisingly, the results indicate that only a few of the growth promoting events induced by CML are fully dependent on mTOR signalling (e.g. hypertrophy). These results advance our understanding of the molecular mechanisms that regulate skeletal muscle mass and should help future studies aimed at identifying targets for therapies that can prevent the loss of muscle mass during conditions such as bedrest, immobilization, and ageing.
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