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Mechanisms of Autophagy Initiation
Annual Review of Biochemistry ( IF 12.1 ) Pub Date : 2017-06-27 00:00:00 , DOI: 10.1146/annurev-biochem-061516-044820
James H. Hurley 1 , Lindsey N. Young 1
Affiliation  

Autophagy is the process of cellular self-eating by a double-membrane organelle, the autophagosome. A range of signaling processes converge on two protein complexes to initiate autophagy: the ULK1 (unc51-like autophagy activating kinase 1) protein kinase complex and the PI3KC3–C1 (class III phosphatidylinositol 3-kinase complex I) lipid kinase complex. Some 90% of the mass of these large protein complexes consists of noncatalytic domains and subunits, and the ULK1 complex has essential noncatalytic activities. Structural studies of these complexes have shed increasing light on the regulation of their catalytic and noncatalytic activities in autophagy initiation. The autophagosome is thought to nucleate from vesicles containing the integral membrane protein Atg9 (autophagy-related 9), COPII (coat protein complex II) vesicles, and possibly other sources. In the wake of reconstitution and super-resolution imaging studies, we are beginning to understand how the ULK1 and PI3KC3–C1 complexes might coordinate the nucleation and fusion of Atg9 and COPII vesicles at the start of autophagosome biogenesis.

中文翻译:


自噬引发的机制

自噬是由双膜细胞器(自噬体)进行细胞自食的过程。一系列信号传导过程收敛于两种蛋白复合物以启动自噬:ULK1(unc51类自噬活化激酶1)蛋白激酶复合物和PI3KC3-C1(III类磷脂酰肌醇3激酶复合物I)脂质激酶复合物。这些大蛋白复合物的质量中约90%由非催化结构域和亚基组成,而ULK1复合物具有必不可少的非催化活性。这些复合物的结构研究为自噬引发中其催化和非催化活性的调节提供了更多的机会。自噬体被认为是从含有完整膜蛋白Atg9(自噬相关蛋白9),COPII(外壳蛋白复合物II)囊泡的囊泡中形成核的,以及其他来源。在重建和超分辨率成像研究之后,我们开始了解在自噬体生物发生开始时,ULK1和PI3KC3-C1复合物如何协调Atg9和COPII囊泡的成核和融合。

更新日期:2017-06-27
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