mTOR regulation of autophagy

被引:1910
作者
Jung, Chang Hwa [1 ]
Ro, Seung-Hyun [1 ]
Cao, Jing [1 ]
Otto, Neil Michael [1 ]
Kim, Do-Hyung [1 ]
机构
[1] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA
来源
FEBS LETTERS | 2010年 / 584卷 / 07期
基金
美国国家卫生研究院;
关键词
Mammalian target of rapamycin; Autophagy-related gene 1; UNC-51-like kinase 1; UNC-51-like kinase 2; Autophagy-related gene 13; PROTEIN-KINASE COMPLEX; INHIBITS CELL-GROWTH; P70; S6; KINASE; SACCHAROMYCES-CEREVISIAE; PHOSPHATIDYLINOSITOL; 3-KINASE; SIGNALING PATHWAYS; BINDING PARTNER; ENDOPLASMIC-RETICULUM; RAG GTPASES; C-ELEGANS;
D O I
10.1016/j.febslet.2010.01.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nutrient starvation induces autophagy in eukaryotic cells through inhibition of TOR (target of rapamycin), an evolutionarily-conserved protein kinase. TOR, as a central regulator of cell growth, plays a key role at the interface of the pathways that coordinately regulate the balance between cell growth and autophagy in response to nutritional status, growth factor and stress signals. Although TOR has been known as a key regulator of autophagy for more than a decade, the underlying regulatory mechanisms have not been clearly understood. This review discusses the recent advances in understanding of the mechanism by which TOR regulates autophagy with focus on mammalian TOR (mTOR) and its regulation of the autophagy machinery. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1287 / 1295
页数:9
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