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向HNRNPA2B1抑制了肠道病毒71在SK-N-SH细胞中的复制

Jing Wu¹, Jian Lu², Lingxiang Mao³

¹Department of Laboratory Medicine, the Affiliated Guangji Hospital of Soochow University, Suzhou Mental Health Center, Suzhou, Jiangsu 215137, China.

|September 16, 2023

概括

肠道病毒71 (EV-71) 感染会增加异质核核核糖核蛋白A2B1 (HNRNPA2B1) 的表达,并促进其从核向细胞质转移. 抑制HNRNPA2B1显著减少神经细胞中的EV-71复制.

科学领域:

病毒学病毒学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

肠道病毒71 (EV-71) 是一个重要的人类病原体.
在EV-71复制中,诸如异质核核核糖核蛋白A2B1 (HNRNPA2B1) 等宿主因子的作用尚未完全理解.
SK-N-SH细胞是一种常用的神经母细胞瘤细胞系,用于研究病毒感染.

研究的目的:

研究HNRNPA2B1对SK-N-SH细胞中EV-71复制的作用.
在EV-71感染期间确定HNRNPA2B1的表达水平和局部化.

主要方法:

实时定量PCR (qRT-PCR) 和西部抹杀 (WB) 用于测量HNRNPA2B1mRNA和蛋白质表达.
免疫光学 (IF) 用于评估核和细胞质内的HNRNPA2B1定位.
使用小干扰RNA (siRNA) 来降低HNRNPA2B1的表达.
病毒RNA,VP1蛋白和病毒标位被量化以评估病毒复制.

主要成果:

EV-71感染显著上调了SK-N-SH细胞中的HNRNPA2B1表达.
在EV-71感染时,HNRNPA2B1蛋白从细胞核重新分配到细胞质.
下调HNRNPA2B1表达明显抑制了EV-71复制,包括病毒RNA,VP1蛋白和病毒标位.

结论:

在支持EV-71复制方面,HNRNPA2B1起着至关重要的作用.
EV-71感染诱导HNRNPA2B1表达和局部化的变化,有利于其细胞质积累.
针对HNRNPA2B1是一个潜在的策略来抑制EV-71的传播.

关键词:

在EV-71中,它是EV-71.这是一个HFMD.这就是HNRNPA2B1B1B1B2B1B1B1B2B1B1B1B1B1B1B1B1B1B1B2B1B2B1B1B2B1B1B2B1B1B1B2B1B2B1B2B2B1B2B1B2B2B2B2B2B2B2B2B2B2B2B2B2B2B2B2B2 细胞 SK-N-SH 细胞.

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