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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BioMed Central
2016
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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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1613593157914591232 |