期刊
JOURNAL OF VIRAL HEPATITIS
卷 19, 期 5, 页码 353-363出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2893.2011.01556.x
关键词
heat shock protein 72; hepatitis C virus; hepatocellular carcinoma; NFAT5; nonstructural 5A; reactive oxygen species
资金
- National Research Laboratory and Biotechnology Development from Ministry of Education, Science and Technology, Korea [ROA-2007-0056700, 2008-2004100]
- Ministry for Health and Welfare, Korea [1020290]
- Korea Health Promotion Institute [1020290] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2008-2004100] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
We identified heat shock protein 72 (Hsp72) as a host factor that was differentially expressed in cells expressing nonstructural 5A (NS5A) protein. To investigate how NS5A modulates Hsp72 in hepatitis C virus (HCV) life cycle, we examined the role of Hsp72 in HCV replication and virus production. NS5A specifically interacted with Hsp72. Both Hsp72 and nuclear factor of activated T cells 5 (NFAT5) levels were increased in cells expressing NS5A protein. Treatments of N-acetylcysteine and glutathione markedly reduced protein levels of both NFAT5 and Hsp72. Knockdown of NFAT5 resulted in decrease in Hsp72 level in cells expressing NS5A. Importantly, silencing of Hsp72 expression resulted in decrease in both RNA replication and virus production in HCV-infected cells. These data indicate that NS5A modulates Hsp72 via NFAT5 and reactive oxygen species activation for HCV propagation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据