Translocase of outer mitochondrial membrane 70 induces interferon response and is impaired by hepatitis C virus NS3

• 笠間, 由里

• 齋藤, 誠

• 高野, 隆

• 西村, 知裕

• 佐藤, 正明

• 原田, 信志

• 小原, 道法

• 小原, 恭子

• Saito, Makoto

• Takano, Takashi

• Satoh, Masaaki

• Wang, Zhongzhi

• Salem Nagla Elwy Salem Ali

• Harada, Shinji

• Kohara, Michinori

抄録

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論文(Article)

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.

http://www.sciencedirect.com/science/article/pii/S0168170211004035

収録刊行物

• Virus Research

  Virus Research 163 (1), 405-409, 2012-01

  Elsevier

キーワード

• HCV
• Tom70
• MAVS
• IFN
• IRF-3
• NS3

詳細情報

• CRID: 1050001337930014336
• NII論文ID: 120004853375
• ISSN: 01681702
• HANDLE: 2298/25748
• Web Site: https://kumadai.repo.nii.ac.jp/records/26629
• 本文言語コード: en
• 資料種別: journal article
• データソース種別:
  • IRDB
  • CiNii Articles