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アイテム
The ASK family kinases differentially mediate type I interferon induction and apoptosis during the antiviral response
http://hdl.handle.net/2261/57531
http://hdl.handle.net/2261/575310cc65585-a863-4c93-8442-9a63415db0d5
| 名前 / ファイル | ライセンス | アクション |
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scisignal.aab1883.pdf (3.7 MB)
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| アイテムタイプ | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2015-08-27 | |||||
| タイトル | ||||||
| タイトル | The ASK family kinases differentially mediate type I interferon induction and apoptosis during the antiviral response | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源 | http://purl.org/coar/resource_type/c_6501 | |||||
| タイプ | journal article | |||||
| 著者 |
Okazaki, Tomohiko
× Okazaki, Tomohiko× Higuchi, Maiko× Takeda, Kohsuke× Iwatsuki-Horimoto, Kiyoko× Kiso, Maki× Miyagishi, Makoto× Yanai, Hideyuki× Kato, Atsushi× Yoneyama, Mitsutoshi× Fujita, Takashi× Taniguchi, Tadatsugu× Kawaoka, Yoshihiro× Ichijo, Hidenori× Gotoh, Yukiko |
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| 著者所属 | ||||||
| 著者所属 | Laboratory of Molecular Biology, Graduate School of Pharmaceutical Sciences, The University of Tokyo | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Division of Cell Regulation, Graduate School of Biomedical Sciences, Nagasaki University | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Molecular Composite Medicine Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST) | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Department of Molecular Immunology and Center for International Research on Integrative Biomedical Systems, Institute of Industrial Science, The University of Tokyo | |||||
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| 言語 | en | |||||
| 著者所属 | Max Planck-The University of Tokyo Center for Integrative Inflammology | |||||
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| 言語 | en | |||||
| 著者所属 | Department of Virology 3, National Institute of Infectious Diseases | |||||
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| 言語 | en | |||||
| 著者所属 | Medical Mycology Research Center, Chiba University | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Department of Special Pathogens, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency | |||||
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| 言語 | en | |||||
| 著者所属 | Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison | |||||
| 著者所属 | ||||||
| 言語 | en | |||||
| 著者所属 | Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Viral infection activates host defense mechanisms, including the production of type I interferon (IFN) and the apoptosis of infected cells. We investigated whether these two antiviral responses were differentially regulated in infected cells. We showed that the mitogen-activated protein kinase (MAPK) kinase kinase (MAPKKK) apoptosis signal–regulating kinase 1 (ASK1) was activated in cells by the synthetic double-stranded RNA analog polyinosinic:polycytidylic acid [poly(I:C)] and by RNA viruses, and that ASK1 played an essential role in both the induction of the gene encoding IFN-β (IFNB) and apoptotic cell death. In contrast, we found that the MAPKKK ASK2, a modulator of ASK1 signaling, was essential for ASK1-dependent apoptosis, but not for inducing IFNB expression. Furthermore, genetic deletion of either ASK1 or ASK2 in mice promoted the replication of influenza A virus in the lung. These results indicated that ASK1 and ASK2 are components of the antiviral defense mechanism and suggested that ASK2 acts as a key modulator that promotes apoptosis rather than the type I IFN response. Because ASK2 is selectively present in epithelium-rich tissues, such as the lung, ASK2-dependent apoptosis may contribute to an antiviral defense in tissues with a rapid repair rate in which cells could be readily replaced. | |||||
| 言語 | en | |||||
| 内容記述 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | UTokyo Research掲載「生きるべきか死ぬべきか」 URI: http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/to-be-or-not-to-be-that-is-the-question.html | |||||
| 言語 | ja | |||||
| 内容記述 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | UTokyo Research "To be, or not to be: That is the question" URI: http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/to-be-or-not-to-be-that-is-the-question.html | |||||
| 言語 | en | |||||
| bibliographic_information |
en : Science signaling 巻 8, 号 388, p. ra78, 発行日 2015-08-04 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 19450877 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 19379145 | |||||
| 書誌レコードID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA12315525 | |||||
| item_2_relation_11 | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | info:doi/10.1126/scisignal.aab1883 | |||||
| 権利 | ||||||
| 権利情報 | © 2015 Authors. | |||||
| item_2_select_14 | ||||||
| 値 | author | |||||
| 出版者 | ||||||
| 出版者 | American Association for the Advancement of Science | |||||
| 関係URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/to-be-or-not-to-be-that-is-the-question.html | |||||
| 関係URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/to-be-or-not-to-be-that-is-the-question.html | |||||
| 関係URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://stke.sciencemag.org/content/8/388/ra78.abstract | |||||
