The nucleocapsid protein of severe acute respiratory syndrome coronavirus inhibits cell cytokinesis and proliferation by interacting with translation elongation factor 1alpha.
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| Abstract |
Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of SARS, an emerging disease characterized by atypical pneumonia. Using a yeast two-hybrid screen with the nucleocapsid (N) protein of SARS-CoV as a bait, the C terminus (amino acids 251 to 422) of the N protein was found to interact with human elongation factor 1-alpha (EF1alpha), an essential component of the translational machinery with an important role in cytokinesis, promoting the bundling of filamentous actin (F-actin). In vitro and in vivo interaction was then confirmed by immuno-coprecipitation, far-Western blotting, and surface plasmon resonance. It was demonstrated that the N protein of SARS-CoV induces aggregation of EF1alpha, inhibiting protein translation and cytokinesis by blocking F-actin bundling. Proliferation of human peripheral blood lymphocytes and other human cell lines was significantly inhibited by the infection of recombinant retrovirus expressing SARS-CoV N protein.
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| Authors | Bing Zhou, Junli Liu, Qiuna Wang, Xuan Liu, Xiaorong Li, Ping Li, Qingjun Ma, Cheng Cao |
| Journal | Journal of virology (J Virol) Vol. 82 Issue 14 Pg. 6962-71 (Jul 2008) ISSN: 1098-5514 [Electronic] United States |
| PMID | 18448518 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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