Ubiquitin, Autophagy and Neurodegenerative Diseases

被引:57
|
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
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
收藏
页数:15
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