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高效的细胞-基质粘附位点拆卸需要NBR1依赖的选择性自噬。

NBR1-dependent selective autophagy is required for efficient cell-matrix adhesion site disassembly.

作者信息

Kenific Candia M, Debnath Jayanta

机构信息

a Department of Pathology and Helen Diller Family Comprehensive Cancer Center , University of California San Francisco , San Francisco , CA , USA.

b Biomedical Sciences Graduate Program , University of California San Francisco , San Francisco , CA , USA.

出版信息

Autophagy. 2016 Oct 2;12(10):1958-1959. doi: 10.1080/15548627.2016.1212789. Epub 2016 Aug 2.

DOI:10.1080/15548627.2016.1212789
PMID:27484104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5079663/
Abstract

Macroautophagy/autophagy has classically been recognized for its vital role in supporting cellular survival during various stresses. However, emerging work has demonstrated that selective autophagy has an impact on diverse cell biological processes by mediating the degradation of various cellular contents during normal cellular homeostasis. We recently established that selective autophagy supports cell migration by promoting the turnover of integrin-based cell-matrix adhesion sites, or focal adhesions (FAs). The autophagy cargo receptor NBR1 acts as a critical mediator of this pathway by promoting targeting of autophagosomes to FAs, leading to their disassembly via the sequestration of FA proteins. Our results demonstrate FAs as a new cellular target for selective autophagy.

摘要

传统上,巨自噬/自噬因其在各种应激过程中支持细胞存活的重要作用而被人们所认识。然而,新出现的研究表明,选择性自噬在正常细胞内稳态期间通过介导各种细胞内容物的降解,对多种细胞生物学过程产生影响。我们最近发现,选择性自噬通过促进基于整合素的细胞-基质黏附位点(即粘着斑,FAs)的周转来支持细胞迁移。自噬货物受体NBR1通过促进自噬体靶向粘着斑,导致粘着斑通过隔离粘着斑蛋白而解体,从而作为该途径的关键介质。我们的结果表明,粘着斑是选择性自噬的一个新的细胞靶点。

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