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本文引用的文献

1
Expanding the host cell ubiquitylation machinery targeting cytosolic .扩展靶向胞质的宿主细胞泛素化机制
EMBO Rep. 2017 Sep;18(9):1572-1585. doi: 10.15252/embr.201643851. Epub 2017 Aug 6.
2
STUB1 regulates TFEB-induced autophagy-lysosome pathway.STUB1调节TFEB诱导的自噬-溶酶体途径。
EMBO J. 2017 Sep 1;36(17):2544-2552. doi: 10.15252/embj.201796699. Epub 2017 Jul 28.
3
Full length RTN3 regulates turnover of tubular endoplasmic reticulum via selective autophagy.全长RTN3通过选择性自噬调节管状内质网的周转。
Elife. 2017 Jun 15;6:e25555. doi: 10.7554/eLife.25555.
4
The Logic of the 26S Proteasome.26S蛋白酶体的逻辑
Cell. 2017 May 18;169(5):792-806. doi: 10.1016/j.cell.2017.04.023.
5
Linear ubiquitination of cytosolic Salmonella Typhimurium activates NF-κB and restricts bacterial proliferation.细胞质型鼠伤寒沙门氏菌的线性泛素化激活 NF-κB 并限制细菌增殖。
Nat Microbiol. 2017 May 8;2:17066. doi: 10.1038/nmicrobiol.2017.66.
6
LUBAC-synthesized linear ubiquitin chains restrict cytosol-invading bacteria by activating autophagy and NF-κB.LUBAC 合成的线性泛素链通过激活自噬和 NF-κB 来限制细胞质入侵细菌。
Nat Microbiol. 2017 May 8;2:17063. doi: 10.1038/nmicrobiol.2017.63.
7
Proteasomal and Autophagic Degradation Systems.蛋白酶体和自噬降解系统。
Annu Rev Biochem. 2017 Jun 20;86:193-224. doi: 10.1146/annurev-biochem-061516-044908. Epub 2017 May 1.
8
Polyglutamine tracts regulate beclin 1-dependent autophagy.聚谷氨酰胺序列调节依赖于贝林1的自噬。
Nature. 2017 May 4;545(7652):108-111. doi: 10.1038/nature22078. Epub 2017 Apr 26.
9
SUMO and the robustness of cancer.SUMO 与癌症的稳健性。
Nat Rev Cancer. 2017 Mar;17(3):184-197. doi: 10.1038/nrc.2016.143. Epub 2017 Jan 30.
10
A Single Legionella Effector Catalyzes a Multistep Ubiquitination Pathway to Rearrange Tubular Endoplasmic Reticulum for Replication.一种嗜肺军团菌效应蛋白催化多步骤泛素化途径,以重排管状内质网用于复制。
Cell Host Microbe. 2017 Feb 8;21(2):169-181. doi: 10.1016/j.chom.2016.12.007. Epub 2016 Dec 29.

泛素信号与自噬。

Ubiquitin signaling and autophagy.

机构信息

From the Institute of Biochemistry II, Goethe University Frankfurt-Medical Faculty, University Hospital, 60590 Frankfurt am Main and.

From the Institute of Biochemistry II, Goethe University Frankfurt-Medical Faculty, University Hospital, 60590 Frankfurt am Main and

出版信息

J Biol Chem. 2018 Apr 13;293(15):5404-5413. doi: 10.1074/jbc.TM117.000117. Epub 2017 Nov 29.

DOI:10.1074/jbc.TM117.000117
PMID:29187595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5900779/
Abstract

Ubiquitination is a widespread post-translational modification that controls multiple steps in autophagy, a major lysosome-mediated intracellular degradation pathway. A variety of ubiquitin chains are attached as selective labels on protein aggregates and dysfunctional organelles, thus promoting their autophagy-dependent degradation. Moreover, ubiquitin modification of autophagy regulatory components is essential to positively or negatively regulate autophagy flux in both non-selective and selective pathways. We review the current findings that elucidate the components, timing, and kinetics of the multivalent role of ubiquitin signals in control of amplitude and selectivity of autophagy pathways as well as their impact on the development of human diseases.

摘要

泛素化是一种广泛存在的翻译后修饰,可控制自噬这一主要溶酶体介导的细胞内降解途径中的多个步骤。各种泛素链作为选择性标签附着在蛋白聚集体和功能失调的细胞器上,从而促进它们的自噬依赖性降解。此外,自噬调节成分的泛素修饰对于正向或负向调节非选择性和选择性途径中的自噬流是必不可少的。我们综述了目前的研究结果,这些结果阐明了泛素信号在控制自噬途径的幅度和选择性方面的多价作用的组成、时间和动力学,以及它们对人类疾病发展的影响。