Emerging Mechanisms in Initiating and Terminating Autophagy

被引:257
作者
Antonioli, Manuela [1 ,2 ]
Di Rienzo, Martina [1 ,3 ]
Piacentini, Mauro [1 ,3 ]
Fimia, Gian Maria [1 ,4 ]
机构
[1] IRCCS, Natl Inst Infect Dis L Spallanzani, I-00149 Rome, Italy
[2] Univ Freiburg, Freiburg Inst Adv Studies FRIAS, D-79104 Freiburg, Germany
[3] Univ Roma Tor Vergata, Dept Biol, I-00173 Rome, Italy
[4] Univ Salento, Dept Biol & Environm Sci & Technol DiSTeBA, I-73100 Lecce, Italy
基金
欧盟第七框架计划;
关键词
BECLIN; 1; INHIBITS AUTOPHAGY; REGULATES AUTOPHAGY; ULK1; COMPLEX; VPS34; COMPLEXES; BCL-2; FAMILY; KINASE; AMBRA1; PHOSPHORYLATION; PROTEINS;
D O I
10.1016/j.tibs.2016.09.008
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 major degradative process activated in a rapid and transient manner to cope with stress conditions. Whether autophagy is beneficial or detrimental depends upon the rate of induction and the appropriateness of the duration. Alterations in both autophagy initiation and termination predispose the cell to death, and affect the execution of other inducible processes such as inflammation. In this review we discuss how stress signaling pathways dynamically control the activity of the autophagy machinery by mediating post-translational modifications and regulatory protein interactions. In particular, we highlight the emerging role of TRIM and CULLIN families of ubiquitin ligases which play opposite roles in the autophagy response by promoting or inhibiting, respectively, the activity of the autophagy initiation complex.
引用
收藏
页码:28 / 41
页数:14
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