ArticleJournal of immunology (Baltimore, Md. : 1950)2016
cFLIPL Interrupts IRF3-CBP-DNA Interactions To Inhibit IRF3-Driven Transcription.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- c-FLIP as a master regulator of immune homeostasis and disease mechanisms.Cell death & disease · 2026Review
- The cell death regulator c-FLIPJournal of molecular medicine (Berlin, Germany) · 2025Article
- Zinc-finger CCHC-type containing protein 8 promotes RNA virus replication by suppressing the type-I interferon responses.Journal of virology · 2024Article
- Review
- Review
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- FLIP(L): the pseudo-caspase.The FEBS journal · 2020Review
- Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-DependentViruses · 2020Review
- Molecular characterisation of ILRUN, a novel inhibitor of proinflammatory and antimicrobial cytokines.Heliyon · 2020Article
- Superoxide induced inhibition of death receptor signaling is mediated via induced expression of apoptosis inhibitory protein cFLIP.Redox biology · 2020Article
- The methyltransferase PRMT6 attenuates antiviral innate immunity by blocking TBK1-IRF3 signaling.Cellular & molecular immunology · 2019Article
- C6orf106 is a novel inhibitor of the interferon-regulatory factor 3-dependent innate antiviral response.The Journal of biological chemistry · 2018Article
- Cellular FLIP long isoform (cFLIPThe Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type I IFN induction is critical for antiviral and anticancer defenses. Proper downregulation of type I IFN is equally important to avoid deleterious imbalances in the immune response. The cellular FLIP long isoform protein (cFLIPL) controls type I IFN production, but opposing publications show it as either an inhibitor or inducer of type I IFN synthesis. Regardless, the mechanistic basis for cFLIPL regulation is unknown. Because cFLIPL is important in immune cell development and proliferation, and is a target for cancer therapies, it is important to identify how cFLIPL regulates type I IFN production. Data in this study show that cFLIPL inhibits IFN regulatory factor 3 (IRF3), a transcription factor central for IFN-β and IFN-stimulated gene expression. This inhibition occurs during virus infection, cellular exposure to polyinosinic-polycytidylic acid, or TBK1 overexpression. This inhibition is independent of capase-8 activity. cFLIPL binds to IRF3 and disrupts IRF3 interaction with its IFN-β promoter and its coactivator protein (CREB-binding protein). Mutational analyses reveal that cFLIPL nuclear localization is necessary and sufficient for inhibitory function. This suggests that nuclear cFLIPL prevents IRF3 enhanceosome formation. Unlike other cellular IRF3 inhibitors, cFLIPL did not degrade or dephosphorylate IRF3. Thus, cFLIPL represents a different cellular strategy to inhibit type I IFN production. This new cFLIPL function must be considered to accurately understand how cFLIPL affects immune system development and regulation.
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Registered trials
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.