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標題: Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease
作者: Lai, C.C.
Jou, M.J.
Huang, S.A.Y.
Li, S.W.
Wan, L.
Tsai, F.J.
Lin, C.W.
關鍵字: 2-DE;3C-like protease;MS;Severe acute respiratory syndrome (SARS);coronavirus;mouse hepatitis-virus;apoptosis-inducing factor;vero e6 cells;sars;coronavirus;hong-kong;rna;transcription;infection;carcinoma;cleavage
Project: Proteomics
期刊/報告no:: Proteomics, Volume 7, Issue 9, Page(s) 1446-1460.
The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W, Lin, K. H., Hsieh, I H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro, could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.
ISSN: 1615-9853
DOI: 10.1002/pmic.200600459
Appears in Collections:分子生物學研究所

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