The Shigella flexneri effector OspI deamidates UBC13 to dampen the inflammatory response
Takahito Sanada,
Minsoo Kim,
Hitomi Mimuro,
Masato Suzuki,
Michinaga Ogawa,
Akiho Oyama,
Hiroshi Ashida,
Taira Kobayashi,
Tomohiro Koyama,
Shinya Nagai,
Yuri Shibata,
Jin Gohda,
Jun-ichiro Inoue,
Tsunehiro Mizushima () and
Chihiro Sasakawa ()
Additional contact information
Takahito Sanada: International Research Center for Infectious Diseases, University of Tokyo, Minato-ku
Minsoo Kim: International Research Center for Infectious Diseases, University of Tokyo, Minato-ku
Hitomi Mimuro: International Research Center for Infectious Diseases, University of Tokyo, Minato-ku
Masato Suzuki: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Michinaga Ogawa: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Akiho Oyama: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Hiroshi Ashida: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Taira Kobayashi: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Tomohiro Koyama: Nippon Institute for Biological Science, 9-2221-1 Shinmachi, Ome, Tokyo 198-0024, Japan
Shinya Nagai: Nippon Institute for Biological Science, 9-2221-1 Shinmachi, Ome, Tokyo 198-0024, Japan
Yuri Shibata: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Jin Gohda: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Jun-ichiro Inoue: Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan
Tsunehiro Mizushima: Picobiology Institute, Graduate School of Life Science, University of Hyogo, 3-2-1 Kouto, Kamigori, Akoh, Hyogo 678-1297, Japan
Chihiro Sasakawa: International Research Center for Infectious Diseases, University of Tokyo, Minato-ku
Nature, 2012, vol. 483, issue 7391, 623-626
Abstract:
Shigella flexneri translocates several virulence factors into host cells during infection; one of these proteins, OspI, is a glutamine deamidase that specifically modifies UBC13, a protein involved in immune signalling.
Date: 2012
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DOI: 10.1038/nature10894
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