Regulation Mechanisms and Signaling Pathways of Autophagy

被引:2876
作者
He, Congcong [1 ]
Klionsky, Daniel J.
机构
[1] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
lysosome; Atg proteins; target of rapamycin; stress; pathogen; transcription; ENDOPLASMIC-RETICULUM STRESS; PHOSPHATIDYLINOSITOL 3-KINASE COMPLEXES; INHIBITS CELL-GROWTH; PROTEIN-KINASE-B; AMINO-ACIDS; BECLIN; SELECTIVE AUTOPHAGY; PREAUTOPHAGOSOMAL STRUCTURE; NONSPECIFIC AUTOPHAGY; MULTIVESICULAR BODIES;
D O I
10.1146/annurev-genet-102808-114910
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Autophagy is a process of self-degradation of cellular components in which double-membrane autophagosomes sequester organelles or portions of cytosol and fuse with lysosomes or vacuoles for breakdown by resident hydrolases. Autophagy is upregulated in response to extra- or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy plays a significant role in human pathologies, including cancer, neurodegeneration, and infectious diseases. We present our current knowledge on the key genes composing the autophagy machinery in eukaryotes from yeast to mammalian cells and the signaling pathways that sense the status of different types of stress and induce autophagy for cell survival and homeostasis. We also review the recent advances on the molecular mechanisms that regulate the autophagy machinery at various levels, from transcriptional activation to post-translational protein modification.
引用
收藏
页码:67 / 93
页数:27
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