RNA recognition and signal transduction by RIG-I-like receptors

Authors

  • Mitsutoshi Yoneyama,

    1. Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.
    2. Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
    3. PRESTO, Japan Science and Technology Agency, Saitama, Japan.
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  • Takashi Fujita

    1. Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.
    2. Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
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Takashi Fujita
Laboratory of Molecular Genetics
Institute for Virus Research, Kyoto University
Shogoinkawahara-cho, Sakyo-ku
Kyoto 606-8507
Japan
Tel.: + 81 75 751 4031
Fax: + 81 75 751 4031
e-mail: tfujita@virus.kyoto-u.ac.jp

Abstract

Summary:  Viral infection is detected by cellular sensor molecules as foreign nucleic acids and initiates innate antiviral responses, including the activation of proinflammatory cytokines and type I interferon (IFN). Recent identification of cytoplasmic viral sensors, such as retinoic acid-inducible gene-I-like receptors (RLRs), highlights their significance in the induction of antiviral innate immunity. Moreover, it is intriguing to understand how they can discriminate endogenous RNA from foreign viral RNA and initiate signaling cascades leading to the induction of type I IFNs. This review focuses on the current understanding of the molecular machinery underlying RNA recognition and subsequent signal transduction by RLRs.

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