Biology and trafficking of ATG9 and ATG16L1, two proteins that regulate autophagosome formation

被引:66
|
作者
Zavodszky, Eszter [1 ]
Vicinanza, Mariella [1 ]
Rubinsztein, David C. [1 ]
机构
[1] Univ Cambridge, Addenbrookes Hosp, Dept Med Genet, Cambridge Inst Med Res, Cambridge CB2 0XY, England
基金
英国惠康基金;
关键词
Autophagy; Atg9; Atg16; Phagophore; Membrane trafficking; GENOME-WIDE ASSOCIATION; SACCHAROMYCES-CEREVISIAE; ENDOPLASMIC-RETICULUM; LC3; LIPIDATION; CONJUGATION SYSTEM; ISOLATION MEMBRANE; CROHN-DISEASE; COMPLEX; YEAST; GOLGI;
D O I
10.1016/j.febslet.2013.04.025
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
Autophagy is a highly conserved intracytoplasmic degradation pathway for proteins, oligomers, organelles and pathogens. It initiates with the formation of a cup-shaped double membrane structure called the phagophore. The membrane origin for autophagosomes has been a key question for the field. ATG9 and ATG16L1, or their yeast orthologues, are key proteins that regulate autophagosome biogenesis, and may be associated with distinct membrane sources. Here we review the biology of autophagy with a focus on ATG16L1 and ATG9, and we summarise the current knowledge of their trafficking in relation to autophagic stimuli and autophagosome formation. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1988 / 1996
页数:9
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