Ubiquitin, Autophagy and Neurodegenerative Diseases

被引：63

作者：

Watanabe, Yoshihisa ^{[1
]}

Taguchi, Katsutoshi ^{[2
]}

Tanaka, Masaki ^{[2
]}

机构：

[1] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Basic Geriatr, Kyoto 6028566, Japan

[2] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Anat & Neurobiol, Kyoto 6028566, Japan

来源：

CELLS | 2020年 / 9卷 / 09期

基金：

日本学术振兴会;

关键词：

ubiquitin; autophagy; neurodegenerative diseases; ubiquitin-proteasome system; autophagy-lysosome pathway; AMYOTROPHIC-LATERAL-SCLEROSIS; STRESS-RESPONSE PATHWAY; ALPHA-SYNUCLEIN; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; TAU-PHOSPHORYLATION; PROTEIN-DEGRADATION; PHASE-SEPARATION; IN-VIVO; A-BETA;

D O I：

10.3390/cells9092022

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Ubiquitin signals play various roles in proteolytic and non-proteolytic functions. Ubiquitin signals are recognized as targets of the ubiquitin-proteasome system and the autophagy-lysosome pathway. In autophagy, ubiquitin signals are required for selective incorporation of cargoes, such as proteins, organelles, and microbial invaders, into autophagosomes. Autophagy receptors possessing an LC3-binding domain and a ubiquitin binding domain are involved in this process. Autophagy activity can decline as a result of genetic variation, aging, or lifestyle, resulting in the onset of various neurodegenerative diseases. This review summarizes the selective autophagy of neurodegenerative disease-associated protein aggregates via autophagy receptors and discusses its therapeutic application for neurodegenerative diseases.

引用

页数：15

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