| SARS-CoV nucleocapsid protein induced apoptosis of COS-1 mediated by the mitochondrial pathway. | |
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MedLine Citation:
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PMID: 17453707 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To investigate the apoptosis effect of SARS coronavirus nucleocapsid protein on cultured cell lines and to explore the possible pathway of apoptosis. pCDNA3.1(-)/his-myc vector containing the SARS coronavirus nucleocapsid gene (N), matric gene (M), spike gene (S) were transfected into COS-1, Huh-7 and HepG2 cells. Apoptosis induced by SARS coronavirus N protein under starvation of serum of COS-1 cells was monitored by Annexin V and electron microscopy assays. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (DeltaPsim) were determined by flow cytometric assay. Cytochrome C, cleaved caspase (cysteine aspartic acid protease)-3, 9, and poly (ADP-ribose) polymerase (PARP) were detected by Western blot. After removal of serum in COS-1 cells, we observed the loss of DeltaPsim, the increase of ROS and cytochrome C release into cytosol and subsequent activation of caspase-3 and PARP cleavage. The pan-caspase inhibitor z-VAD-fmk can block the activation of caspase 3, 9 and PARP cleavage. In conclusion, SARS coronavirus N protein can induce apoptosis of COS-1 cells by activating mitochondrial pathway. SARS coronavirus M, S protein can not induce apoptosis in COS-1, HepG2 and Huh-7 and SARS coronavirus N protein can not induce apoptosis in HepG2 and Huh-7 by methods used in this study. |
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Authors:
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Lu Zhang; Lai Wei; Dong Jiang; Jianghua Wang; Xu Cong; Ran Fei |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Artificial cells, blood substitutes, and immobilization biotechnology Volume: 35 ISSN: 1073-1199 ISO Abbreviation: Artif Cells Blood Substit Immobil Biotechnol Publication Date: 2007 |
Date Detail:
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Created Date: 2007-04-24 Completed Date: 2007-05-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9431307 Medline TA: Artif Cells Blood Substit Immobil Biotechnol Country: United States |
Other Details:
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Languages: eng Pagination: 237-53 Citation Subset: IM |
Affiliation:
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Hepatology Institute, Peking University, People's Hospital, Beijing, People's Republic of China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis* Blotting, Western COS Cells Carcinoma, Hepatocellular Caspase 9 / metabolism Cell Line, Tumor Cercopithecus aethiops Cytochromes c / metabolism Flow Cytometry Genetic Vectors Humans Liver Neoplasms Membrane Glycoproteins / genetics, metabolism Membrane Potential, Mitochondrial / physiology Microscopy, Electron Mitochondria / physiology*, ultrastructure, virology* Nucleocapsid Proteins / genetics*, metabolism Phosphatidylserines / metabolism Reactive Oxygen Species / metabolism SARS Virus / genetics* Transfection Viral Envelope Proteins / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Membrane Glycoproteins; 0/Nucleocapsid Proteins; 0/Phosphatidylserines; 0/Reactive Oxygen Species; 0/Viral Envelope Proteins; 0/nucleocapsid protein, Coronavirus; 107476-75-5/spike glycoprotein, coronavirus; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspase 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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