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Epithelial Cell Infection Analyses with Shigella
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通过Shigella病毒毒性因子IpaJJ对N-myristoyl修饰的蛋白质分解性消除
Nikolay Burnaevskiy1, Thomas G Fox, Daniel A Plymire
1Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8816, USA.
Nature
|March 29, 2013
概括
西格拉柔性菌的入侵等离子体抗原J (IpaJ) 从宿主蛋白质中去除N-myristoyl修饰物. 这种脱化破坏了宿主细胞的信号和分泌,揭示了一种新的细菌致病机制.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 微生物学 微生物学
背景情况:
- 蛋白N-myristoylation是一种对蛋白质功能和细胞信号传递至关重要的保存修饰.
- 基基团调解关键的蛋白质-蛋白质和蛋白质-膜相互作用.
- 病原细菌可能会向蛋白质修饰来操纵宿主细胞.
研究的目的:
- 识别和描述涉及修改宿主蛋白功能的新型细菌效应蛋白.
- 阐明Shigella flexneri IpaJ影响宿主细胞过程的机制.
- 为了研究蛋白质脱化在细菌病原发生中的作用.
主要方法:
- 酵母基因查以确定IpaJ基底.
- 质谱测量用于分析蛋白质分裂部位.
- 生物化学测试以确认蛋白酶活性和基质特异性.
主要成果:
- 石格拉柔性菌的入侵等离子体抗原J (IpaJ) 被确定为一种囊蛋白酶.
- IpaJ特别分裂N-基化蛋白,包括ADP-核糖化因子1 (ARF1).
- 通过IpaJ介导的脱基酶抑制宿主细胞的分泌,并影响各种细胞功能.
结论:
- IpaJ采用一种新的局部特异性蛋白质脱化机制来破坏宿主细胞的信号传递.
- 这种细菌策略为宿主分泌途径的抑制提供了新的途径.
- 这些发现揭示了一种未被识别的致病机制,涉及消除N-myristoyl蛋白修饰.
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