2024-03-29T08:39:40Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/447452023-11-21T06:59:52Zhdl_2115_20040hdl_2115_121The ubiquitin ligase Riplet is essential for RIG-I-dependent innate immune responses to RNA virus infection.The essential role of a ubiquitin ligase, Riplet, in RIG-I-dependent antiviral innate immune responsesOshiumi, HiroyukiMiyashita, MoekoInoue, NaokazuOkabe, MasaruMatsumoto, MisakoSeya, TsukasaRNA virus infection is recognized by the RIG-I-like receptors RIG-I and MDA5, which induce antiviral responses including the production of type I inter- ferons (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, macro- phages, 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 dispens- able 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.Cell pressJournal Articleapplication/pdfhttp://hdl.handle.net/2115/44745https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/44745/3/CHM8-6_496-509.pdf1931-3128AA12230659Cell Host & Microbe864965092010-12-16enginfo:pmid/21147464info:doi/10.1016/j.chom.2010.11.008author