ArticleNature communications2015
TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- TIF1γ regulates stability of regulatory T cells during inflammation.Nature immunology · 2026Article
- Soluble SIGLEC1 as a biomarker of disease activity in idiopathic inflammatory myopathies.Rheumatology (Oxford, England) · 2026Article
- Chromatin-mediated anticipatory control of type I interferon production in plasmacytoid dendritic cells.Immunity · 2026Article
- Autoantibody internalization in myositis skeletal muscle: Emerging evidence, mechanistic insights, and therapeutic relevance.Autoimmunity reviews · 2026Review
- A Quinoxaline Derivative as a New Therapeutic Agent for Sepsis through Suppression of TLR4 Signaling Pathways.Inflammation · 2025Article
- Protective Effects of a Dihydrodiazepine Against Endotoxin Shock Through Suppression of TLR4/NF-κB/IRF3 Signaling Pathways.Inflammation · 2025Article
- SUMO operates from a unique long tandem repeat to keep innate immunity in check.Nucleic acids research · 2025Article
- Article
- Dazukibart for dermatomyositis: expanding the therapeutic arsenal.Annals of translational medicine · 2025Article
- The emerging role of protein L-lactylation in metabolic regulation and cell signalling.Nature metabolism · 2025Review
- The SP140-RESIST pathway regulates interferon mRNA stability and antiviral immunity.bioRxiv : the preprint server for biology · 2025Article
- The TRIM33 Bromodomain Recognizes Histone Lysine Lactylation.ACS chemical biology · 2024Article
- Recent Updates on the Pathogenesis of Inflammatory Myopathies.Current rheumatology reports · 2024Review
- TRIM32 inhibits Venezuelan equine encephalitis virus infection by targeting a late step in viral entry.PLoS pathogens · 2024Article
- Pathological autoantibody internalisation in myositis.Annals of the rheumatic diseases · 2024Article
- Genome-scale CRISPR-Cas9 screen identifies host factors as potential therapeutic targets for SARS-CoV-2 infection.iScience · 2024Article
- TRIM33 plays a critical role in regulating dendritic cell differentiation and homeostasis by modulating Irf8 and Bcl2l11 transcription.Cellular & molecular immunology · 2024Article
- TRIM32 inhibits Venezuelan Equine Encephalitis Virus Infection by targeting a late step in viral entry.bioRxiv : the preprint server for biology · 2024Article
- Genome-wide screening identifies Trim33 as an essential regulator of dendritic cell differentiation.Science immunology · 2024Article
- Pathogenic autoantibody internalization in myositis.medRxiv : the preprint server for health sciences · 2024Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite its importance during viral or bacterial infections, transcriptional regulation of the interferon-β gene (Ifnb1) in activated macrophages is only partially understood. Here we report that TRIM33 deficiency results in high, sustained expression of Ifnb1 at late stages of toll-like receptor-mediated activation in macrophages but not in fibroblasts. In macrophages, TRIM33 is recruited by PU.1 to a conserved region, the Ifnb1 Control Element (ICE), located 15 kb upstream of the Ifnb1 transcription start site. ICE constitutively interacts with Ifnb1 through a TRIM33-independent chromatin loop. At late phases of lipopolysaccharide activation of macrophages, TRIM33 is bound to ICE, regulates Ifnb1 enhanceosome loading, controls Ifnb1 chromatin structure and represses Ifnb1 gene transcription by preventing recruitment of CBP/p300. These results characterize a previously unknown mechanism of macrophage-specific regulation of Ifnb1 transcription whereby TRIM33 is critical for Ifnb1 gene transcription shutdown.
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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.