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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16268

    Title: Interferon antagonist function of Japanese encephalitis virus NS4A and its interaction with DEAD-box RNA helicase DDX42
    Authors: 林振文;LIN, CHENG-WEN;Cheng, Chieh-Wen;Yang, Tsuey-Ching;Li, Shih-Wein;Cheng, Mei-Hsiu;Wan, Lei;Lin, Ying-Ju;Lai, Chih-Ho;Lin, Wei-Yong;Kao, Ming-Ching
    Contributors: 生物科技學系
    Keywords: Japanese encephalitis virus;NS4A;IFN antagonist;RNA helicase DDX42
    Date: 2008-05
    Issue Date: 2012-11-23 17:10:43 (UTC+8)
    Abstract: The interferon (IFN) antagonists of Japanese encephalitis virus (JEV) proteins contribute to the JE pathogenesis. Most flavivirus non-structural (NS) proteins correlate with virus-induced inflammation and immune escape. NS4A proteins of West Nile virus and dengue type 2 virus have been demonstrated to inhibit IFN signaling. In this study, JEV NS4A without the C-terminal 2K domain has been demonstrated to partially block activation of an IFN-stimulated response element (ISRE)-based cis-reporter by IFN-alpha/beta. In addition, JEV NS4A significantly inhibited the phosphorylation levels of STAT1 and STAT2, but not TYK2 in the IFN-treated cells. Moreover, the N-terminus of a RNA helicase DDX42 protein identified using a phage display human brain cDNA library have been demonstrated to specifically bind to JEV NS4A in vitro using a co-immunoprecipitation assay. The interaction between JEV NS4A and RNA helicase DDX42 showed partial co-localization in human medulloblastoma TE-671 cells by confocal microscopy. Importantly, the expression of N-terminal DDX42 is able to overcome JEV-induced antagonism of IFN responses. Therefore, these results show that JEV NS4A without the C-terminal 2K domain is associated with modulation of the IFN response and the interaction of JEV NS4A with RNA helicase DDX42 could be important for JE pathogenesis.
    Relation: VIRUS RESEARCH, V.137 N.1:49–55.
    Appears in Collections:[生物科技學系] 期刊論文

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