Cullin-RING ligases in regulation of autophagy

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, a...

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Main Authors: Cui, Danrui, Xiong, Xiufang, Zhao, Yongchao
Format: Online
Language:English
Published: BioMed Central 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4902950/
id pubmed-4902950
recordtype oai_dc
spelling pubmed-49029502016-06-12 Cullin-RING ligases in regulation of autophagy Cui, Danrui Xiong, Xiufang Zhao, Yongchao Review 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. BioMed Central 2016-06-10 /pmc/articles/PMC4902950/ /pubmed/27293474 http://dx.doi.org/10.1186/s13008-016-0022-5 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Cui, Danrui
Xiong, Xiufang
Zhao, Yongchao
spellingShingle Cui, Danrui
Xiong, Xiufang
Zhao, Yongchao
Cullin-RING ligases in regulation of autophagy
author_facet Cui, Danrui
Xiong, Xiufang
Zhao, Yongchao
author_sort Cui, Danrui
title Cullin-RING ligases in regulation of autophagy
title_short Cullin-RING ligases in regulation of autophagy
title_full Cullin-RING ligases in regulation of autophagy
title_fullStr Cullin-RING ligases in regulation of autophagy
title_full_unstemmed Cullin-RING ligases in regulation of autophagy
title_sort cullin-ring ligases in regulation of autophagy
description 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.
publisher BioMed Central
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4902950/
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