ArticleNature immunology2010
The transcription factor MafB antagonizes antiviral responses by blocking recruitment of coactivators to the transcription factor IRF3.
Article in Nature immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- Genome-wide RNAi screen reveals a new role of a WNT/CTNNB1 signaling pathway as negative regulator of virus-induced innate immune responses.PLoS pathogens · 2013Trial
- Microglial Prrc2a regulates microglia-neuron interaction in cerebellum and motor functions in mice.iScience · 2025Article
- Article
- Type I interferon signalling and interferon-responsive microglia in health and disease.The FEBS journal · 2025Review
- Mycobacterium tuberculosis impairs protective cytokine production via transcription factor MafB manipulation.PLoS pathogens · 2025Article
- Microarray Analysis Reveals Sepsis Is a Syndrome with Hyperactivity of TH17 Immunity, with Over-Presentation of the Treg Cell Cytokine TGF-β.Current issues in molecular biology · 2025Article
- Article
- Macrophage re-programming by JAK inhibitors relies on MAFB.Cellular and molecular life sciences : CMLS · 2024Article
- MAFB shapes human monocyte-derived macrophage response to SARS-CoV-2 and controls severe COVID-19 biomarker expression.JCI insight · 2023Article
- Myeloid-specific KDM6B inhibition sensitizes glioblastoma to PD1 blockade.Nature cancer · 2023Article
- What's happening where when SARS-CoV-2 infects: are TLR7 and MAFB sufficient to explain patient vulnerability?Immunity & ageing : I & A · 2022Review
- Transcription factor MAFB controls type I and II interferon response-mediated host immunity inFrontiers in microbiology · 2022Article
- Myeloid cells in COVID-19 microenvironment.Signal transduction and targeted therapy · 2021Review
- Dendritic Cells: Versatile Players in Renal Transplantation.Frontiers in immunology · 2021Review
- Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-DependentViruses · 2020Review
- Kidney dendritic cells: fundamental biology and functional roles in health and disease.Nature reviews. Nephrology · 2020Review
- SARS-CoV-2 Proteins Exploit Host's Genetic and Epigenetic Mediators for the Annexation of Key Host Signaling Pathways.Frontiers in molecular biosciences · 2020Article
- MAFB and MAF Transcription Factors as Macrophage Checkpoints for COVID-19 Severity.Frontiers in immunology · 2020Article
- Loss of MafA and MafB expression promotes islet inflammation.Scientific reports · 2019Article
- Transcriptional and Epigenetic Regulation of Microglia in Health and Disease.Trends in molecular medicine · 2019Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Viral infection induces type I interferons (IFN-alpha and IFN-beta) that recruit unexposed cells in a self-amplifying response. We report that the transcription factor MafB thwarts auto-amplification by a metastable switch activity. MafB acted as a weak positive basal regulator of transcription at the IFNB1 promoter through activity at transcription factor AP-1-like sites. Interferon elicitors recruited the transcription factor IRF3 to the promoter, whereupon MafB acted as a transcriptional antagonist, impairing the interaction of coactivators with IRF3. Mathematical modeling supported the view that prepositioning of MafB on the promoter allows the system to respond rapidly to fluctuations in IRF3 activity. Higher expression of MafB in human pancreatic islet beta cells might increase cellular vulnerability to viral infections associated with the etiology of type 1 diabetes.
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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.