@article{oai:kumadai.repo.nii.ac.jp:00026629,
 author = {笠間, 由里 and Kasama, Yuri and 齋藤, 誠 and 高野, 隆 and 西村, 知裕 and Nishimura, Tomohiro and 佐藤, 正明 and 原田, 信志 and 小原, 道法 and 小原, 恭子 and Kohara, Kyoko and Tsukiyama-Kohara, Kyoko and 笠間, 由里 and Kasama, Yuri and Saito, Makoto and Takano, Takashi and 西村, 知裕 and Nishimura, Tomohiro and Satoh, Masaaki and Wang, Zhongzhi and Salem Nagla Elwy Salem Ali and Harada, Shinji and Kohara, Michinori and 小原, 恭子 and Kohara, Kyoko and Tsukiyama-Kohara, Kyoko},
 issue = {1},
 journal = {Virus Research},
 month = {Jan},
 note = {application/pdf, 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},
 pages = {405--409},
 title = {Translocase of outer mitochondrial membrane 70 induces interferon response and is impaired by hepatitis C virus NS3},
 volume = {163},
 year = {2012},
 yomi = {カサマ, ユリ and ニシムラ, トモヒロ and コハラ, キョウコ and カサマ, ユリ and ニシムラ, トモヒロ and コハラ, キョウコ}
}