Cullin-RING ligases in regulation of autophagy

被引:57
作者
Cui, Danrui [1 ,2 ]
Xiong, Xiufang [2 ]
Zhao, Yongchao [1 ,2 ]
机构
[1] Zhejiang Univ, Sch Med, Key Lab Combined Multiorgan Transplantat, Minist Publ Hlth,Affiliated Hosp 1, 79 Qing Chun Rd, Hangzhou 310003, Zhejiang, Peoples R China
[2] Zhejiang Univ, Sch Med, Inst Translat Med, 268 Kai Xuan Rd, Hangzhou 310029, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
CRL E3 ligase; UPS; Autophagy; mTOR; Ubiquitin; NEDD8; ATG; E3 UBIQUITIN LIGASE; CHAPERONE-MEDIATED AUTOPHAGY; TUMOR-SUPPRESSOR; BETA-TRCP; SKELETAL-MUSCLE; PROTEASOME PATHWAY; PROTEIN-DEGRADATION; INHIBITS AUTOPHAGY; SIGNALING PATHWAY; COP9; SIGNALOSOME;
D O I
10.1186/s13008-016-0022-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cullin-RING ligases (CRLs), the largest E3 ubiquitin ligase family, promote ubiquitination and degradation of various cellular key regulators involved in a broad array of physiological and pathological processes, including cell cycle progression, signal transduction, transcription, cardiomyopathy, and tumorigenesis. Autophagy, an intracellular catabolic reaction that delivers cytoplasmic components to lysosomes for degradation, is crucial for cellular metabolism and homeostasis. The dysfunction of autophagy has been proved to associate with a variety of human diseases. Recent evidences revealed the emerging roles of CRLs in the regulation of autophagy. In this review, we will focus mainly on recent advances in our understandings of the regulation of autophagy by CRLs and the cross-talk between CRLs and autophagy, two degradation systems. We will also discuss the pathogenesis of human diseases associated with the dysregulation of CRLs and autophagy. Finally, we will discuss current efforts and future perspectives on basic and translational research on CRLs and autophagy.
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页数:14
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