Mammalian Autophagy: How Does It Work?

被引：531

作者：

Bento, Carla F. ^{[1
]}

Renna, Maurizio ^{[1
]}

Ghislat, Ghita ^{[1
]}

Puri, Claudia ^{[1
]}

Ashkenazi, Avraham ^{[1
]}

Vicinanza, Mariella ^{[1
]}

Menzies, Fiona M. ^{[1
]}

Rubinsztein, David C. ^{[1
]}

机构：

[1] Univ Cambridge, Wellcome Trust, Cambridge Inst Med Res, Dept Med Genet, MRC Bldg,Cambridge Biomed Campus, Cambridge CB2 0XY, England

来源：

ANNUAL REVIEW OF BIOCHEMISTRY, VOL 85 | 2016年 / 85卷

关键词：

autophagy; lysosome; endocytosis; autophagosome biogenesis; membrane trafficking; structural biology; STARVATION-INDUCED AUTOPHAGY; INITIATING KINASE ULK1; BECLIN; ATG12-ATG5; CONJUGATE; SELECTIVE AUTOPHAGY; INHIBITS AUTOPHAGY; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; LYSOSOME FUSION; RAT HEPATOCYTES;

D O I：

10.1146/annurev-biochem-060815-014556

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 conserved intracellular pathway that delivers cytoplasmic contents to lysosomes for degradation via double-membrane autophagosomes. Autophagy substrates include organelles such as mitochondria, aggregate-prone proteins that cause neurodegeneration and various pathogens. Thus, this pathway appears to be relevant to the pathogenesis of diverse diseases, and its modulation may have therapeutic value. Here, we focus on the cell and molecular biology of mammalian autophagy and review the key proteins that regulate the process by discussing their roles and how these may be modulated by posttranslational modifications. We consider the membrane-trafficking events that impact autophagy and the questions relating to the sources of autophagosome membrane(s). Finally, we discuss data from structural studies and some of the insights these have provided.

引用

页码：685 / 713

页数：29

共 173 条

[1] Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulum [J].