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细胞内病原体对RAB5调控的自噬的破坏

Subversion of RAB5-regulated autophagy by the intracellular pathogen .

作者信息

Rikihisa Yasuko

机构信息

a Department of Veterinary Biosciences, The Ohio State University , Columbus , OH , USA.

出版信息

Small GTPases. 2019 Sep;10(5):343-349. doi: 10.1080/21541248.2017.1332506. Epub 2017 Jul 5.

DOI:10.1080/21541248.2017.1332506
PMID:28650718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6748376/
Abstract

Intracellular pathogens often exploit RAB functions to establish a safe haven in which to survive and proliferate. , an obligatory intracellular bacterium, resides in specialized membrane-bound inclusions that have early endosome-like characteristics, e.g., resident RAB5 GTPase and RAB5 effectors, including VPS34 (the catalytic subunit of class III phosphatidylinositol 3-kinase), but the inclusions lack late endosomal or lysosomal markers. Within inclusions, obtains host-derived nutrients by inducing RAB5-regulated autophagy using translocated factor-1 deployed by its type IV secretion system. This manipulation of RAB5 by a bacterial molecule offers a simple strategy for to avoid destruction in lysosomes and obtain nutrients, membrane components, and a homeostatic intra-host-cell environment in which to grow.

摘要

细胞内病原体常常利用RAB功能来建立一个安全的生存和增殖场所。嗜肺军团菌是一种专性细胞内细菌,存在于具有早期内体样特征的特殊膜结合包涵体中,例如驻留的RAB5 GTP酶和RAB5效应蛋白,包括VPS34(III类磷脂酰肌醇3激酶的催化亚基),但这些包涵体缺乏晚期内体或溶酶体标记物。在包涵体内,嗜肺军团菌通过利用其IV型分泌系统分泌的转运因子1诱导RAB5调节的自噬来获取宿主来源的营养物质。细菌分子对RAB5的这种操控为嗜肺军团菌提供了一种简单的策略,以避免在溶酶体中被破坏,并获得营养物质、膜成分以及一个可在其中生长的宿主细胞内稳态环境。

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