ArticleEMBO reports2016
RNF123 has an E3 ligase-independent function in RIG-I-like receptor-mediated antiviral signaling.
Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- The Crohn's disease-related RNF123 prevents NLRP3 inflammasome assembly by catalyzing unanchored K63-linked ubiquitination on NEK7.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- RNF20 dynamically regulates RIG-I and MDA5 transcription and degradation via nucleocytoplasmic translocation to balance antiviral signaling.PLoS pathogens · 2026Article
- A Comprehensive Review of the Genetic and Epigenetic Contributions to the Development of Fibromyalgia.Biomedicines · 2023Review
- The RING finger protein family in health and disease.Signal transduction and targeted therapy · 2022Review
- Genome-wide association study identifiesAnnals of the rheumatic diseases · 2021Article
- Transcriptome-Wide Association Study Provides Insights Into the Genetic Component of Gene Expression in Anxiety.Frontiers in genetics · 2021Article
- Ring finger protein 219 regulates inflammatory responses by stabilizing sirtuin 1.British journal of pharmacology · 2020Article
- Role of RING-Type E3 Ubiquitin Ligases in Inflammatory Signalling and Inflammatory Bowel Disease.Mediators of inflammation · 2020Review
- Regulation of cGAS- and RLR-mediated immunity to nucleic acids.Nature immunology · 2020Review
- Intracellular sensing of viral genomes and viral evasion.Experimental & molecular medicine · 2019Review
- ARRDC4 regulates enterovirus 71-induced innate immune response by promoting K63 polyubiquitination of MDA5 through TRIM65.Cell death & disease · 2017Article
- RNF123 has an E3 ligase-independent function in RIG-I-like receptor-mediated antiviral signaling.EMBO reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are cytoplasmic sensors crucial for recognizing different species of viral RNAs, which triggers the production of type I interferons (IFNs) and inflammatory cytokines. Here, we identify RING finger protein 123 (RNF123) as a negative regulator of RIG-I and MDA5. Overexpression of RNF123 inhibits IFN-β production triggered by Sendai virus (SeV) and encephalomyocarditis picornavirus (EMCV). Knockdown or knockout of endogenous RNF123 potentiates IFN-β production triggered by SeV and EMCV, but not by the sensor of DNA viruses cGAS RNF123 associates with RIG-I and MDA5 in both endogenous and exogenous cases in a viral infection-inducible manner. The SPRY and coiled-coil, but not the RING, domains of RNF123 are required for the inhibitory function. RNF123 interacts with the N-terminal CARD domains of RIG-I/MDA5 and competes with the downstream adaptor VISA/MAVS/IPS-1/Cardif for RIG-I/MDA5 CARD binding. These findings suggest that RNF123 functions as a novel inhibitor of innate antiviral signaling mediated by RIG-I and MDA5, a function that does not depend on its E3 ligase activity.
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