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oai:kumadai.repo.nii.ac.jp:00026629 2025-05-01T07:16:01Z 413:443

Translocase of outer mitochondrial membrane 70 induces interferon response and is impaired by hepatitis C virus NS3 Kasama, Yuri 笠間, 由里 カサマ, ユリ Saito, Makoto 齋藤, 誠 サイトウ, マコト Takano, Takashi 高野, 隆 タカノ, タカシ Nishimura, Tomohiro 西村, 知裕 ニシムラ, トモヒロ Satoh, Masaaki 佐藤, 正明 サトウ, マサアキ Wang, Zhongzhi Salem Nagla Elwy Salem Ali Harada, Shinji 原田, 信志 ハラダ, シンジ Kohara, Michinori 小原, 道法 コハラ, ミチノリ Kohara, Kyoko 小原, 恭子 コハラ, キョウコ open access (C) 2012 Elsevier 493 HCV Tom70 MAVS IFN IRF-3 NS3 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. Elsevier 2012-01 eng journal article AM http://hdl.handle.net/2298/25748 https://kumadai.repo.nii.ac.jp/records/26629 https://doi.org/10.1016/j.virusres.2011.10.009 0168-1702 Virus Research 163 1 405 409 https://kumadai.repo.nii.ac.jp/record/26629/files/Virus Research2012.VOL163.pdf application/pdf 564.3 kB 2020-03-02