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学科主题基础医学
Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2
Zhang, Hao1,2; Feng, Hai1; Luo, Lingqi1; Zhou, Qi1; Luo, Zhijun3; Peng, Yihong1,2
关键词HSV-2 Viral replication MEK1 MEK2 ERK siRNA
刊名VIRUS RESEARCH
2010-06-01
DOI10.1016/j.virusres.2010.02.007
150期:1-2页:22-27
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Virology
研究领域[WOS]Virology
关键词[WOS]ERK SIGNALING PATHWAY ; MAP KINASE ; RAS/RAF/MEK/ERK PATHWAY ; CELL-PROLIFERATION ; MAMMALIAN-CELLS ; INHIBITION ; ACTIVATION ; GROWTH ; INFECTION ; APOPTOSIS
英文摘要

During infection, viruses hijack various host cell components and programs for their amplification, among which is the canonical ERK signaling pathway, mainly consisting of three tiered serine/threonine kinases, Rat, MEK and ERK. MEK1 and MEK2 are two isoforms of the kinase operating immediately upstream of ERK, and connecting Raf and ERK by phosphorylating ERR. Previous studies have suggested that different isoforms of MEK have distinct biological functions, although their in vitro kinase function may be redundant. However, little is known about the isoform-specific effects of these kinases on viral propagation. In this study, we showed that herpes simplex virus type 2 (HSV-2) infection of human embryonic kidney (HER) 293 cells induced a sustained activation of ERK1/2. Inhibition of this ERK activation by U0126, a specific inhibitor of MEK1/2, severely impaired virus production. A similar reduction of virus production was also seen following transfection of cells with siRNAs for MEK1/2. Interestingly, a specific knockdown of MEK1 with siRNAs caused a marked inhibition of viral titers, viral proteins and virus-induced cytopathic effect (CPE), whereas silencing MEK2 had little effect. Therefore, our results demonstrate that MEK1 and MEK2 act differently and that HSV-2 hijacks host MEK1 for its own amplification. To our knowledge, this is the first report showing inhibition of HSV-2 replication by targeting human MEK1. This study also suggests that MEK1 could be a potential target for anti-HSV-2 therapy, which may minimize damage to the host cells engendered by targeting both MEK1 and MEK2. (C) 2010 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000277821200003
项目编号2007AA02Z317 ; 30470084
资助机构National High-Tech Research and Development Program of China (863 Program) ; National Natural Science Foundation of China
引用统计
被引频次:24[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/50049
专题北京大学基础医学院_病原生物学系
北京大学基础医学院
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Microbiol, Beijing 100191, Peoples R China
2.Peking Univ, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
3.Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA
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GB/T 7714
Zhang, Hao,Feng, Hai,Luo, Lingqi,et al. Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2[J]. VIRUS RESEARCH,2010,150(1-2):22-27.
APA Zhang, Hao,Feng, Hai,Luo, Lingqi,Zhou, Qi,Luo, Zhijun,&Peng, Yihong.(2010).Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2.VIRUS RESEARCH,150(1-2),22-27.
MLA Zhang, Hao,et al."Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2".VIRUS RESEARCH 150.1-2(2010):22-27.
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