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ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/46762

Title: ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses
Authors: Hayakawa, Sumio Browse this author
Shiratori, Souichi Browse this author
Yamato, Hiroaki Browse this author
Kameyama, Takeshi Browse this author
Kitatsuji, Chihiro Browse this author
Kashigi, Fumi Browse this author
Goto, Showhey Browse this author
Kameoka, Shoichiro Browse this author
Fujikura, Daisuke Browse this author
Yamada, Taisho Browse this author
Mizutani, Tatsuaki Browse this author
Kazumata, Mika Browse this author
Sato, Maiko Browse this author
Tanaka, Junji Browse this author
Asaka, Masahiro Browse this author
Ohba, Yusuke Browse this author
Miyazaki, Tadaaki Browse this author →KAKEN DB
Imamura, Masahiro Browse this author
Takaoka, Akinori Browse this author
Issue Date: Jan-2011
Publisher: Nature Publishing Group
Journal Title: Nature Immunology
Volume: 12
Issue: 1
Start Page: 37
End Page: 44
Publisher DOI: 10.1038/ni.1963
PMID: 21102435
Abstract: The poly(ADP-ribose) polymerases (PARPs) participate in various processes. Here, we report that the PARP-13/ZAP shorter isoform (hereafter called ZAPS), rather than the full length protein, is selectively induced by 3pRNA, and functions as a potent stimulator of retinoic acid-inducible gene-I (RIG-I)-mediated interferon (IFN) responses in human cells. ZAPS associates with RIG-I to promote the oligomerization and ATPase activity of RIG-I, leading to robust activation of IRF3 and NF-κB pathways. Disruption of the PARP-13/ZAP gene, ZC3HAV1, severely abrogated the induction of IFN-α, IFN-β and other cytokines upon viral infection. These results indicate that ZAPS is a key regulator of RIG-I signaling during the innate antiviral immune response, suggesting its possible use as a therapeutic target for viral control.
Type: article (author version)
URI: http://hdl.handle.net/2115/46762
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 高岡 晃教

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