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The ubiquitin ligase Riplet is essential for RIG-I-dependent innate immune responses to RNA virus infection.

Abstract
RNA virus infection is recognized by the RIG-I-like receptors RIG-I and MDA5, which induce antiviral responses including the production of type I interferons (IFNs) and proinflammatory cytokines. RIG-I is regulated by Lys63-linked polyubiquitination, and three E3 ubiquitin ligases, RNF125, TRIM25, and Riplet, are reported to target RIG-I for ubiquitination. To examine the importance of Riplet in vivo, we generated Riplet-deficient mice. Fibroblasts, macrophages, and conventional dendritic cells from Riplet-deficient animals were defective for the production of IFN and other cytokines in response to infection with several RNA viruses. However, Riplet was dispensable for the production of IFN in response to B-DNA and DNA virus infection. Riplet deficiency abolished RIG-I activation during RNA virus infection, and the mutant mice were more susceptible to vesicular stomatitis virus infection than wild-type mice. These data indicate that Riplet is essential for regulating RIG-I-mediated innate immune response against RNA virus infection in vivo.
AuthorsHiroyuki Oshiumi, Moeko Miyashita, Naokazu Inoue, Masaru Okabe, Misako Matsumoto, Tsukasa Seya
JournalCell host & microbe (Cell Host Microbe) Vol. 8 Issue 6 Pg. 496-509 (Dec 16 2010) ISSN: 1934-6069 [Electronic] United States
PMID21147464 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2010 Elsevier Inc. All rights reserved.
Chemical References
  • CARD Signaling Adaptor Proteins
  • Interferon Type I
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Receptors, Cell Surface
  • Robo3 protein, mouse
  • Rnf135 protein, mouse
  • Ubiquitin-Protein Ligases
Topics
  • Animals
  • CARD Signaling Adaptor Proteins (physiology)
  • Cells, Cultured
  • DNA Viruses (immunology, physiology)
  • Dendritic Cells (immunology, virology)
  • Fibroblasts (immunology, virology)
  • Immunity, Innate
  • Interferon Type I (biosynthesis)
  • Macrophages (immunology, virology)
  • Male
  • Membrane Proteins (physiology)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nerve Tissue Proteins (physiology)
  • RNA Virus Infections (immunology)
  • RNA Viruses (immunology, physiology)
  • Receptors, Cell Surface
  • Signal Transduction
  • Ubiquitin-Protein Ligases (genetics, physiology)

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