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  1. 120 薬学系研究科・薬学部
  2. 60 薬科学専攻
  3. 1206010 学術雑誌論文
  1. 0 資料タイプ別
  2. 10 学術雑誌論文
  3. 014 自然科学

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/2261/57531
0cc65585-a863-4c93-8442-9a63415db0d5
名前 / ファイル ライセンス アクション
scisignal.aab1883.pdf scisignal.aab1883.pdf (3.7 MB)
Item type 学術雑誌論文 / Journal Article(1)
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
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

WEKO 2586

Okazaki, Tomohiko

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Higuchi, Maiko

× Higuchi, Maiko

WEKO 2587

Higuchi, Maiko

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Takeda, Kohsuke

× Takeda, Kohsuke

WEKO 2588

Takeda, Kohsuke

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Iwatsuki-Horimoto, Kiyoko

× Iwatsuki-Horimoto, Kiyoko

WEKO 2589

Iwatsuki-Horimoto, Kiyoko

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Kiso, Maki

× Kiso, Maki

WEKO 2590

Kiso, Maki

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Miyagishi, Makoto

× Miyagishi, Makoto

WEKO 2591

Miyagishi, Makoto

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Yanai, Hideyuki

× Yanai, Hideyuki

WEKO 2592

Yanai, Hideyuki

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Kato, Atsushi

× Kato, Atsushi

WEKO 2593

Kato, Atsushi

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Yoneyama, Mitsutoshi

× Yoneyama, Mitsutoshi

WEKO 2594

Yoneyama, Mitsutoshi

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Fujita, Takashi

× Fujita, Takashi

WEKO 2595

Fujita, Takashi

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Taniguchi, Tadatsugu

× Taniguchi, Tadatsugu

WEKO 2596

Taniguchi, Tadatsugu

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Kawaoka, Yoshihiro

× Kawaoka, Yoshihiro

WEKO 2597

Kawaoka, Yoshihiro

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Ichijo, Hidenori

× Ichijo, Hidenori

WEKO 2598

Ichijo, Hidenori

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Gotoh, Yukiko

× Gotoh, Yukiko

WEKO 2599

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
著者所属 Division of Cell Regulation, Graduate School of Biomedical Sciences, Nagasaki University
著者所属
著者所属 Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo
著者所属
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
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
著者所属
著者所属 Max Planck-The University of Tokyo Center for Integrative Inflammology
著者所属
著者所属 Department of Virology 3, National Institute of Infectious Diseases
著者所属
著者所属 Medical Mycology Research Center, Chiba University
著者所属
著者所属 Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University
著者所属
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
著者所属 ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency
著者所属
著者所属 Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison
著者所属
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.
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
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
書誌情報 Science signaling

巻 8, 号 388, p. ra78, 発行日 2015-08-04
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
DOI
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.
著者版フラグ
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
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