ArticleThe Journal of biological chemistry2018
C6orf106 is a novel inhibitor of the interferon-regulatory factor 3-dependent innate antiviral response.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Variation in antiviral immunity and inflammation pathways precedes HIV-1 infection in a high-risk African cohort.The Journal of clinical investigation · 2026Article
- Genetic Contribution to Medium-Term Disease Activity in Multiple Sclerosis.Molecular neurobiology · 2025Article
- Zinc-finger CCHC-type containing protein 8 promotes RNA virus replication by suppressing the type-I interferon responses.Journal of virology · 2024Article
- ILRUN Promotes Atherosclerosis Through Lipid-Dependent and Lipid-Independent Factors.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Structural mechanism of protein recognition by the FW domain of autophagy receptor Nbr1.Nature communications · 2022Article
- ILRUN Downregulates ACE2 Expression and Blocks Infection of Human Cells by SARS-CoV-2.Journal of virology · 2021Article
- Inflammation status modulates the effect of host genetic variation on intestinal gene expression in inflammatory bowel disease.Nature communications · 2021Article
- Pulmonary Mesenchymal Stem Cells in Mild Cases of COVID-19 Are Dedicated to Proliferation; In Severe Cases, They Control Inflammation, Make Cell Dispersion, and Tissue Regeneration.Frontiers in immunology · 2021Article
- Article
- Linking Lipid-Related Transcription and Cardiovascular Disease Through GWAS.Circulation research · 2020Article
- Molecular characterisation of ILRUN, a novel inhibitor of proinflammatory and antimicrobial cytokines.Heliyon · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host recognition of intracellular viral RNA and subsequent induction of cytokine signaling are tightly regulated at the cellular level and are a target for manipulation by viruses and therapeutics alike. Here, we characterize chromosome 6 ORF 106 (C6orf106) as an evolutionarily conserved inhibitor of the innate antiviral response. C6orf106 suppresses the synthesis of interferon (IFN)-α/β and proinflammatory tumor necrosis factor (TNF) α in response to the dsRNA mimic poly(I:C) and to Sendai virus infection. Unlike canonical inhibitors of antiviral signaling, C6orf106 blocks interferon-regulatory factor 3 (IRF3) and, to a lesser extent, NF-κB activity without modulating their activation, nuclear translocation, cellular expression, or degradation. Instead, C6orf106 interacts with IRF3 and inhibits IRF3 recruitment to type I IFN promoter sequences while also reducing the nuclear levels of the coactivator proteins p300 and CREB-binding protein (CBP). In summary, we have defined C6orf106 as a negative regulator of antiviral immunity that blocks IRF3-dependent cytokine production via a noncanonical and poorly defined mechanism. This work presents intriguing implications for antiviral immunity, autoimmune disorders, and cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.