ArticleImmunity2024
Collaboration between distinct SWI/SNF chromatin remodeling complexes directs enhancer selection and activation of macrophage inflammatory genes.
Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Virtual screening and cellular validation of dolutegravir as a BRD9 inhibitor for attenuating pyroptosis in peritoneal mesothelial cells.Renal failure · 2026Article
- MNS induces antiviral protection and suppresses inflammation.Annals of medicine · 2026Article
- PBRM1 Deficiency in Microglia Leads to Excessive Neurogenesis and Autism-Like Behaviors via the CCL5-CCR1/5-β-catenin Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Genomic Stress and DNA Repair During Macrophage Differentiation and Inflammatory Activation.International journal of molecular sciences · 2026Review
- Delineating SWI/SNF gene and subtype expression in cancer.Epigenetics & chromatin · 2026Article
- PBRM1-dependent PBAF targeting is required for EMT and metastasis in breast cancer.Science advances · 2026Article
- Quantitative Control of Transposable Elements: From Genome Plasticity to Immune Regulatory Circuits.Cell biochemistry and function · 2026Review
- Versatile SMAD2 and SMAD3 epitope-tagged mouse models for genomic profiling of TGFβ signaling: Uncovering GDF9-SMAD2/3 targets.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses.bioRxiv : the preprint server for biology · 2026Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Role of PBAF and Mediator kinase module in the RELA-dependent activation ofFrontiers in immunology · 2026Article
- The SWI/SNF chromatin-remodeling subunit DPF2 regulates macrophage inflammation in intestinal injury via the CACNA1D-mediated MAPK pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Persistent Activation of Endothelial Cells is Linked to Thrombosis and Inflammation in Cerebral Cavernous Malformation Disease.bioRxiv : the preprint server for biology · 2025Article
- Mutation of SMARCA4 Induces Cancer Cell-Intrinsic Defects in the Enhancer Landscape and Resistance to Immunotherapy.Cancer research · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Macrophages elicit immune responses to pathogens through induction of inflammatory genes. Here, we examined the role of three variants of the SWI/SNF nucleosome remodeling complex-cBAF, ncBAF, and PBAF-in the macrophage response to bacterial endotoxin (lipid A). All three SWI/SNF variants were prebound in macrophages and retargeted to genomic sites undergoing changes in chromatin accessibility following stimulation. Cooperative binding of all three variants associated with de novo chromatin opening and latent enhancer activation. Isolated binding of ncBAF and PBAF, in contrast, associated with activation and repression of active enhancers, respectively. Chemical and genetic perturbations of variant-specific subunits revealed pathway-specific regulation in the activation of lipid A response genes, corresponding to requirement for cBAF and ncBAF in inflammatory and interferon-stimulated gene (ISG) activation, respectively, consistent with differential engagement of SWI/SNF variants by signal-responsive transcription factors. Thus, functional diversity among SWI/SNF variants enables increased regulatory control of innate immune transcriptional programs, with potential for specific therapeutic targeting.
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