The role of the Atg1/ULK1 complex in autophagy regulation

被引：845

作者：

Mizushima, Noboru ^{[1
]}

机构：

[1] Tokyo Med & Dent Univ, Dept Physiol & Cell Biol, Tokyo 1138519, Japan

来源：

CURRENT OPINION IN CELL BIOLOGY | 2010年 / 22卷 / 02期

关键词：

INHIBITS CELL-GROWTH; AXONAL ELONGATION; KINASE COMPLEX; PROTEIN; YEAST; ATG1; TOR; BINDING; ULK1; MTOR;

D O I：

10.1016/j.ceb.2009.12.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The Atg1/ULK complex plays an essential role in the initiation of autophagy: receiving signals of cellular nutrient status, recruiting downstream Atg proteins to the autophagosome formation site, and governing autophagosome formation. Recent studies of mammalian Atg1 homologs (ULK1 and ULK2) have identified several novel interacting proteins, FIP200, mAtg13, and Atg101. FIP200 and Atg101 are not conserved in Saccharomyces cerevisiae, despite the high conservation rates of other downstream Atg proteins between the yeast and mammals. Furthermore, through studies of the Atg1/ULK1 complex, the molecular mechanism by which (m)TORC1 regulates autophagy is now being clarified in detail.

引用

页码：132 / 139

页数：8

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