E3 Ubiquitin Ligase RNF114 Inhibits Innate Immune Response to Red-Spotted Grouper Nervous Necrosis Virus Infection in Sea Perch by Targeting MAVS and TRAF3 to Mediate Their Degradation

نویسندگان

چکیده

Abstract RIG-I–like receptor (RLR)–mediated antiviral signaling is critical to trigger the immune response virus infection; however, responses are also tightly regulated avoid uncontrolled production of type I IFN by various mechanisms, including ubiquitination. In this study, an E3 ubiquitin ligase ring finger protein 114 (RNF114) from sea perch (Lateolabrax japonicus) (LjRNF114) was identified as a suppressor RLR pathways during red-spotted grouper nervous necrosis (RGNNV) infection. RGNNV infection promoted expression LjRNF114. Overexpression LjRNF114 enhanced replication, whereas knockdown led opposite effects. Type induced suppressed LjRNF114, which dependent on its activity. Moreover, inhibited promoter activation key molecules in pathways. We observed interactions between and both mitochondrial (MAVS) TNFR-associated factor 3 (TRAF3). Domain mapping experiments indicated that RING interacting motif domains were required for interaction with TRAF3 MAVS. found targeted MAVS K27- K48-linked ubiquitination degradation, resulting inhibition production. Taken together, our study reveals, knowledge, novel mechanism targets promotes negatively regulate pathways, promoting viral

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2021

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.2000083