P70-S6激酶1
安普克
核糖体蛋白s6
mTORC1型
生物
蛋白激酶A
PI3K/AKT/mTOR通路
核糖体s6激酶
激酶
细胞生物学
TOR信号
调节器
雷帕霉素的作用靶点
信号转导
纺神星
AMP活化蛋白激酶
核糖体蛋白
磷酸化
基因
遗传学
核糖体
核糖核酸
肾
作者
Colin Selman,Jennifer M. A. Tullet,Daniela Wieser,Elaine E. Irvine,Steven J. Lingard,Agharul I. Choudhury,Marc Claret,Hind Al‐Qassab,Danielle Carmignac,Faruk Ramadani,Angela Woods,Iain C. A. F. Robinson,Eugene F. Schuster,Rachel L. Batterham,Sara C. Kozma,George Thomas,David Carling,Klaus Okkenhaug,Janet M. Thornton,Linda Partridge,David Gems,Dominic J. Withers
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2009-10-01
卷期号:326 (5949): 140-144
被引量:1067
标识
DOI:10.1126/science.1177221
摘要
Mimicking Caloric Restriction The extended life span and resistance to age-related diseases in animals exposed to caloric restriction has focused attention on the biochemical mechanisms that produce these effects. Selman et al. (p. 140 ; see the Perspective by Kaeberlein and Kapahi ) explored the role of the mammalian ribosomal protein S6 kinase 1 (S6K1), which regulates protein translation and cellular energy metabolism. Female knockout mice lacking expression of S6K1 showed characteristics of animals exposed to caloric restriction, including improved health and increased longevity. The beneficial effects included reduced fat mass in spite of increased food intake. Thus, inhibition of signaling pathways activated by S6K1 might prove beneficial in protecting against age-related disease.
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