Abstract
Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carrier Proteins / antagonists & inhibitors
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Carrier Proteins / genetics
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Carrier Proteins / metabolism
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Cell Line, Tumor
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Encephalomyocarditis virus / physiology
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Gene Expression Regulation*
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HEK293 Cells
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HeLa Cells
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Host-Pathogen Interactions*
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Humans
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Interferon-beta / genetics*
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Interferon-beta / metabolism
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Promoter Regions, Genetic
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RNA, Small Interfering / genetics
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RNA, Small Interfering / metabolism
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Sendai virus / physiology
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Signal Transduction
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TNF Receptor-Associated Factor 3 / genetics*
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TNF Receptor-Associated Factor 3 / metabolism
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TNF Receptor-Associated Factor 6 / genetics*
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TNF Receptor-Associated Factor 6 / metabolism
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Ubiquitin-Protein Ligases / antagonists & inhibitors
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Ubiquitin-Protein Ligases / genetics*
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Ubiquitin-Protein Ligases / metabolism
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Ubiquitination
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Zinc Fingers
Substances
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Carrier Proteins
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RNA, Small Interfering
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TNF Receptor-Associated Factor 3
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TNF Receptor-Associated Factor 6
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TRAF3 protein, human
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Interferon-beta
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RNF114 protein, human
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RNF125 protein, human
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RNF138 protein, human
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RNF166 protein, human
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Ubiquitin-Protein Ligases