Translocase of outer mitochondrial membrane 70 induces interferon response and is impaired by hepatitis C virus NS3
| Autor: | Masaaki Satoh, Tomohiro Nishimura, Takashi Takano, Makoto Saito, Salem Nagla Elwy Salem Ali, Michinori Kohara, Yuri Kasama, Zhongzhi Wang, Shinji Harada, Kyoko Tsukiyama-Kohara |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Cancer Research
NS3 Hepatitis C virus viruses Hepacivirus Viral Nonstructural Proteins Cleavage (embryo) medicine.disease_cause IFN Mitochondrial Membrane Transport Proteins Outer mitochondrial membrane Interferon Virology Mitochondrial Precursor Protein Import Complex Proteins Immune Tolerance medicine Humans Translocase Immune Evasion biology Tom70 IRF-3 Signal transducing adaptor protein virus diseases Hep G2 Cells MAVS Molecular biology digestive system diseases Infectious Diseases Mitochondrial Membranes HCV Hepatocytes biology.protein Phosphorylation Interferons medicine.drug |
| Zdroj: | Virus Research. 163(1):405-409 |
| ISSN: | 0168-1702 |
| Popis: | Hepatitis C virus (HCV) elevated expression of the translocase of outer mitochondrial membrane 70 (Tom70). Interestingly, overexpression of Tom70 induces interferon (IFN) synthesis in hepatocytes, and it was impaired by HCV. Here, we addressed the mechanism of this impairment. The HCV NS3/4A protein induced Tom70 expression. The HCV NS3 protein interacted in cells, and cleaved the adapter protein mitochondrial anti-viral signaling (MAVS). Ectopic overexpression of Tom70 could not inhibit this cleavage. As a result, IRF-3 phosphorylation was impaired and IFN-β induction was suppressed. These results indicate that MAVS works upstream of Tom70 and the cleavage of MAVS by HCV NS3 protease suppresses signaling of IFN induction. |
| Databáze: | OpenAIRE |
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