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Anatomy of autophagy: from the beginning to the end.自噬的结构:从开始到结束。
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2
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本文引用的文献

1
The Vici Syndrome Protein EPG5 Is a Rab7 Effector that Determines the Fusion Specificity of Autophagosomes with Late Endosomes/Lysosomes.Vici 综合征蛋白 EPG5 是 Rab7 的效应物,决定了自噬体与晚期内体/溶酶体融合的特异性。
Mol Cell. 2016 Sep 1;63(5):781-95. doi: 10.1016/j.molcel.2016.08.021.
2
The Intrinsically Disordered Protein Atg13 Mediates Supramolecular Assembly of Autophagy Initiation Complexes.内在无序蛋白 Atg13 介导自噬起始复合物的超分子组装。
Dev Cell. 2016 Jul 11;38(1):86-99. doi: 10.1016/j.devcel.2016.06.015.
3
Autophagosome-lysosome fusion in neurons requires INPP5E, a protein associated with Joubert syndrome.神经元中的自噬体-溶酶体融合需要INPP5E,一种与乔布综合征相关的蛋白质。
EMBO J. 2016 Sep 1;35(17):1853-67. doi: 10.15252/embj.201593148. Epub 2016 Jun 23.
4
Cholesterol and ORP1L-mediated ER contact sites control autophagosome transport and fusion with the endocytic pathway.胆固醇和 ORP1L 介导的内质网接触位点控制自噬体运输,并与内吞途径融合。
Nat Commun. 2016 Jun 10;7:11808. doi: 10.1038/ncomms11808.
5
An ER-Localized SNARE Protein Is Exported in Specific COPII Vesicles for Autophagosome Biogenesis.内质网定位的 SNARE 蛋白通过特定的 COPII 囊泡输出以进行自噬体生物发生。
Cell Rep. 2016 Feb 23;14(7):1710-1722. doi: 10.1016/j.celrep.2016.01.047. Epub 2016 Feb 11.
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Structure and flexibility of the endosomal Vps34 complex reveals the basis of its function on membranes.内体Vps34复合物的结构与灵活性揭示了其在膜上发挥功能的基础。
Science. 2015 Oct 9;350(6257):aac7365. doi: 10.1126/science.aac7365.
7
ATG14 promotes membrane tethering and fusion of autophagosomes to endolysosomes.ATG14促进自噬体与内溶酶体的膜拴系和融合。
Nature. 2015 Apr 23;520(7548):563-6. doi: 10.1038/nature14147. Epub 2015 Feb 9.
8
Structure of the human autophagy initiating kinase ULK1 in complex with potent inhibitors.与强效抑制剂结合的人类自噬起始激酶ULK1的结构
ACS Chem Biol. 2015 Jan 16;10(1):257-61. doi: 10.1021/cb500835z. Epub 2015 Jan 6.
9
PLEKHM1 regulates autophagosome-lysosome fusion through HOPS complex and LC3/GABARAP proteins.PLEKHM1 通过 HOPS 复合物和 LC3/GABARAP 蛋白调节自噬体-溶酶体融合。
Mol Cell. 2015 Jan 8;57(1):39-54. doi: 10.1016/j.molcel.2014.11.006. Epub 2014 Dec 11.
10
Phosphatidylinositol 3-kinase and COPII generate LC3 lipidation vesicles from the ER-Golgi intermediate compartment.磷脂酰肌醇3激酶和COPII从内质网-高尔基体中间区室产生LC3脂化囊泡。
Elife. 2014 Nov 28;3:e04135. doi: 10.7554/eLife.04135.

自噬的结构:从开始到结束。

Anatomy of autophagy: from the beginning to the end.

机构信息

Department of Food Science, College of Food Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.

Department of Ophthalmology, UT Southwestern Medical Center, Dallas, TX, 75390, USA.

出版信息

Cell Mol Life Sci. 2018 Mar;75(5):815-831. doi: 10.1007/s00018-017-2657-z. Epub 2017 Sep 22.

DOI:10.1007/s00018-017-2657-z
PMID:28939950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11105611/
Abstract

Autophagy is a highly regulated process in eukaryotes to maintain homeostasis and manage stress responses. Understanding the regulatory mechanisms and key players involved in autophagy will provide critical insights into disease-related pathogenesis and potential clinical treatments. In this review, we describe the hallmark events involved in autophagy, from its initiation, to the final destruction of engulfed targets. Furthermore, based on structural and biochemical data, we evaluate the roles of key players in these processes and provide rationale as to how they control autophagic events in a highly ordered manner.

摘要

自噬是真核生物中一种高度调控的过程,用于维持体内平衡和管理应激反应。了解自噬过程中的调节机制和关键参与者将为疾病相关发病机制和潜在的临床治疗提供重要的见解。在这篇综述中,我们描述了自噬涉及的标志性事件,从其起始到被吞噬目标的最终破坏。此外,根据结构和生化数据,我们评估了这些过程中关键参与者的作用,并提供了它们如何以高度有序的方式控制自噬事件的基本原理。