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    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/3280


    Title: Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
    Authors: 林振文(Cheng-Wen Lin)*;(Kuan-Hsun Lin);(Tsung-Han Hsieh);(Shi-Yi Shiu);(Jeng-Yi Li)
    Contributors: 健康照護學院醫學檢驗生物技術學系;中國附醫檢驗醫學部
    Keywords: SARS-coronavirus;3CLpro;apoptosis;reactive oxygen species;nuclear factor-kappa B signalling
    Date: 2006-04
    Issue Date: 2009-08-20 18:29:07 (UTC+8)
    Abstract: The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CLpro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CLpro-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CLpro-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CLpro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.
    Relation: FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY 46(3):375~380
    Appears in Collections:[Department of Medical Laboratory Science and Biotechnology ] Journal articles

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