Zc3h12a is an RNase essential for controlling immune responses by regulating mRNA decay

Kazufumi Matsushita, Osamu Takeuchi, Daron M. Standley, Yutaro Kumagai, Tatsukata Kawagoe, Tohru Miyake, Takashi Satoh, Hiroki Kato, Tohru Tsujimura, Haruki Nakamura and Shizuo Akira ()
Additional contact information
Kazufumi Matsushita: Laboratory of Host Defense,
Osamu Takeuchi: Laboratory of Host Defense,
Daron M. Standley: Laboratory of Systems Immunology, WPI Immunology Frontier Research Center,
Yutaro Kumagai: Laboratory of Host Defense,
Tatsukata Kawagoe: Laboratory of Host Defense,
Tohru Miyake: Laboratory of Host Defense,
Takashi Satoh: Laboratory of Host Defense,
Hiroki Kato: Laboratory of Host Defense,
Tohru Tsujimura: Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan
Haruki Nakamura: Research Center for Structural and Functional Proteomics, Institute for Protein Research, Osaka University, 3-2 Yamada-oka, Suita, Osaka 565-0871, Japan
Shizuo Akira: Laboratory of Host Defense,

Nature, 2009, vol. 458, issue 7242, 1185-1190

Abstract: The Zc3h12a gene in innate immunity Here the zinc finger protein encoded by the Zc3h12a gene is shown to be a ribonuclease with an essential role in modulating innate immune responses. Zc3h12a is inducible by Toll-like receptors, and this new work suggests that it inhibits autoimmune disease by controlling the degradation of mRNAs encoding proinflammatory cytokines.

Date: 2009
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DOI: 10.1038/nature07924

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