The role of the Atg1/ULK1 complex in autophagy regulation
The role of the Atg1/ULK1 complex in autophagy regulation
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DOI：
10.1016/j.ceb.2009.12.004
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发表时间：
2010-04-01
影响因子：
7.5
通讯作者：
Mizushima, Noboru
中科院分区：
文献类型：
--
作者：
Mizushima, Noboru
Atg1/ULK 复合物在自噬的启动中发挥着重要作用：接收细胞营养状态的信号，将下游 Atg 蛋白招募到自噬体形成位点，并控制自噬体的形成。最近对哺乳动物 Atg1 同源物（ULK1 和 ULK2）的研究发现了几种新型相互作用蛋白：FIP200、mAtg13 和 Atg101。尽管酵母和哺乳动物之间其他下游 Atg 蛋白的保守率很高，但 FIP200 和 Atg101 在酿酒酵母中并不保守。此外，通过对Atg1/ULK1复合物的研究，(m)TORC1调节自噬的分子机制现已被详细阐明。
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.