virus-infection or 5′ppp-rna activates antiviral signal through redistribution of ips-1 mediated by mfn1病毒感染或5u2032ppp-rna激活抗病毒信号通过mfn1 ips-1介导的重新分配.pdfVIP
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virus-infection or 5′ppp-rna activates antiviral signal through redistribution of ips-1 mediated by mfn1病毒感染或5u2032ppp-rna激活抗病毒信号通过mfn1 ips-1介导的重新分配
Virus-Infection or 5 9ppp-RNA Activates Antiviral Signal
through Redistribution of IPS-1 Mediated by MFN1
1,2,3 1 1,2 1,2 1
Kazuhide Onoguchi , Koji Onomoto , Shiori Takamatsu , Michihiko Jogi , Azumi Takemura , Shiho
1 4 3 5,6 1,2
Morimoto , Ilkka Julkunen , Hideo Namiki , Mitsutoshi Yoneyama , Takashi Fujita *
1 Department of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan, 2 Graduate School of Biostudies, Kyoto University, Yoshida-Konoe Sakyo,
Kyoto, Japan, 3 Graduate School of Science and Engineering, Waseda University, Tokyo, Japan, 4 Department of Vaccination and Immune Protection, National Institute for
Health and Welfare, Helsinki, Finland, 5 Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chuo-ku, Chiba, Japan, 6 PRESTO, Japan
Science and Technology Agency, Saitama, Japan
Abstract
In virus-infected cells, RIG-I-like receptor (RLR) recognizes cytoplasmic viral RNA and triggers innate immune responses
including production of type I and III interferon (IFN) and the subsequent expression of IFN-inducible genes. Interferon-b
promoter stimulator 1 (IPS-1, also known as MAVS, VISA and Cardif) is a downstream molecule of RLR and is expressed on
the outer membrane of mitochondria. While it is known that the location of IPS-1 is essential to its function, its underlying
mechanism is unknown. Our aim in this study was to delineate the function of mitochondria so as to identify more precisely
its role in innate immunity. In doing so we discovered that viral infecti
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