ArticleCellular & molecular immunology2024
SENP6 restricts the IFN-I-induced signaling pathway and antiviral activity by deSUMOylating USP8.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SENP5 enhances antiviral innate immunity by promoting AURKA-dependent STAT2 phosphorylation.Cell communication and signaling : CCS · 2026Article
- SENP6 Restrains NLRP3 Inflammasome Activation via DeSUMOylation-Driven K48-Linked Ubiquitination of NLRP3 in Acute Lung Injury.Research (Washington, D.C.) · 2026Article
- USP8-Governed MDA5 Homeostasis Promotes Innate Immunity and Autoimmunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- RNF149 modulates the type I IFN innate antiviral immune responses through degrading IRF3.PLoS pathogens · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
Type I interferon (IFN-I) exhibits broad-spectrum antiviral properties and is commonly employed in clinical for the treatment of viral infections. In this study, we unveil SENP6 as a potent regulator of IFN-I antiviral activity. SENP6 does not impact the production of IFN-I induced by viruses but rather modulates IFN-I-activated signaling. Mechanistically, SENP6 constitutively interacts with USP8 and inhibits the SUMOylation of USP8, consequently restricting the interaction between USP8 and IFNAR2. The dissociation of USP8 from IFNAR2 enhances IFNAR2 ubiquitination and degradation, thus attenuating IFN-I antiviral activity. Correspondingly, the downregulation of SENP6 promotes the interaction between USP8 and IFNAR2, leading to a reduction in IFNAR2 ubiquitination and, consequently, an enhancement in IFN-I-induced signaling. This study deciphers a critical deSUMOylation-deubiquitination crosstalk that finely regulates the IFN-I response to viral infection.
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Registered trials
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