Artikel
Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus-infected cells
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Autoren
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Tetsuya Mizutani
- Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashimurayama, Tokyo 208-0011, Japan Phone: 81-42-561-0771, Fax: 81-42-564-4881
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Shuetsu Fukushi
- Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan
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Shigeru Morikawa
- Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan
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Masayuki Saijo
- Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan
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Ichiro Kurane
- Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan
| Veröffentlicht: | 17. Juni 2004 |
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Gliederung
Text
Severe acute respiratory syndrome (SARS) has become a global public health emergency. Understanding the molecular mechanisms of SARS-induced cytopathic effects (CPEs) is a rational approach to prevention of SARS, and an understanding of the cellular stress responses induced by viral infection is important for understanding the CPEs. Polyclonal antibodies, which recognized nucleocapsid (N) and membrane (M) proteins, detected viral N and M proteins in virus-infected Vero E6 cells at least 6 and 12 h post-infection (h.p.i.), respectively. Furthermore, detection of DNA ladder and cleaved caspase 3 in the virus-infected cells at 24 h.p.i. indicated that SARS-CoV infection induced apoptotic cell death. Phosphorylation of p38 MAPK was significantly up-regulated at 18 h.p.i. in SARS-CoV-infected cells. The downstream targets of p38 MAPK, MAPKAPK-2, HSP-27, CREB, and eIF4E, were phosphorylated in virus-infected cells. These results indicate that the p38 MAPK signaling pathway is important for the response to SARS-CoV-infection.
