ArticleScience signaling2011
The specificity of innate immune responses is enforced by repression of interferon response elements by NF-κB p50.
Article in Science signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 94 citations in OpenAlex.
- Engineering IL-4 resistant proinflammatory human myeloid cells for cancer immunotherapy.Molecular oncology · 2026Article
- The polymerized protein response (PPR) is activated by genetic variants that polymerize in the ER and is mediated by NFκBp50.Nature communications · 2026Article
- Distinct roles for NF-κB in hematopoietic stem cells and the bone marrow milieu in promoting hematopoietic aging.Cell reports · 2025Article
- Gene regulatory logic of the interferon-β enhancer is characterized by two selectively deployed modes of transcription factor synergy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Analogue information processing in NF-κB gene regulatory system.Royal Society open science · 2025Article
- Dendritic cell maturation in cancer.Nature reviews. Cancer · 2025Review
- NF-κB RelB suppresses the inflammatory gene expression programs of dendritic cells by competing with RelA for binding to target gene promoters.Cell discovery · 2025Article
- Striking a balance: new perspectives on homeostatic dendritic cell maturation.Nature reviews. Immunology · 2025Review
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Biophysical characterization of RelA-p52 NF-κB dimer-A link between the canonical and the non-canonical NF-κB pathway.Protein science : a publication of the Protein Society · 2024Article
- The regulation of NFKB1 on CD200R1 expression and their potential roles in Parkinson's disease.Journal of neuroinflammation · 2024Article
- TIANA: transcription factors cooperativity inference analysis with neural attention.BMC bioinformatics · 2024Article
- IL-22 in Atopic Dermatitis.Cells · 2024Review
- Selective regulation of a defined subset of inflammatory and immunoregulatory genes by an NF-κB p50-IκBζ pathway.Genes & development · 2024Article
- The Blueprint of Logical Decisions in a NF-κB Signaling System.ACS omega · 2024Article
- Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis.Cell reports. Medicine · 2024Article
- Direct immunoactivation by chemotherapeutic drugs in cancer treatment.Advanced therapeutics · 2023Article
- RelB-deficient autoinflammatory pathology presents as interferonopathy, but in mice is interferon-independent.The Journal of allergy and clinical immunology · 2023Article
- The correlation between primary open-angle glaucoma (POAG) and gut microbiota: a pilot study towards predictive, preventive, and personalized medicine.The EPMA journal · 2023Article
- X-ray Crystallographic Study of Preferred Spacing by the NF-κB p50 Homodimer on κB DNA.Biomolecules · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The specific binding of transcription factors to cognate sequence elements is thought to be critical for the generation of specific gene expression programs. Members of the nuclear factor κB (NF-κB) and interferon (IFN) regulatory factor (IRF) transcription factor families bind to the κB site and the IFN response element (IRE), respectively, of target genes, and they are activated in macrophages after exposure to pathogens. However, how these factors produce pathogen-specific inflammatory and immune responses remains poorly understood. Combining top-down and bottom-up systems biology approaches, we have identified the NF-κB p50 homodimer as a regulator of IRF responses. Unbiased genome-wide expression and biochemical and structural analyses revealed that the p50 homodimer repressed a subset of IFN-inducible genes through a previously uncharacterized subclass of guanine-rich IRE (G-IRE) sequences. Mathematical modeling predicted that the p50 homodimer might enforce the stimulus specificity of composite promoters. Indeed, the production of the antiviral regulator IFN-β was rendered stimulus-specific by the binding of the p50 homodimer to the G-IRE-containing IFNβ enhancer to suppress cytotoxic IFN signaling. Specifically, a deficiency in p50 resulted in the inappropriate production of IFN-β in response to bacterial DNA sensed by Toll-like receptor 9. This role for the NF-κB p50 homodimer in enforcing the specificity of the cellular response to pathogens by binding to a subset of IRE sequences alters our understanding of how the NF-κB and IRF signaling systems cooperate to regulate antimicrobial immunity.
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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.