ArticleProceedings of the National Academy of Sciences of the United States of America2009
Opposing effects of SWI/SNF and Mi-2/NuRD chromatin remodeling complexes on epigenetic reprogramming by EBF and Pax5.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 140 citations in OpenAlex.
- Epigenetic regulation of humoral immunity: molecular mechanisms, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- B-lineage commitment is dependent on a reversible epigenetic switch.Genes & development · 2026Article
- A novel mutant allele of Mta3 in the mouse: genetic analysis of roles in immunity and androgen biology.G3 (Bethesda, Md.) · 2025Article
- Chromatin interaction-based annotation of regulatory elements reveals dynamic promoter-enhancer interactions in lymphocyte development.iScience · 2025Article
- The nucleosome remodeling and deacetylase-SWItch/sucrose non-fermentable antagonism regulates the coordinated activation of epithelial-to-mesenchymal transition and inflammation in oral cancer.Journal of the National Cancer Institute · 2025Article
- The role of MBD2 in immune cell development, function, and autoimmune diseases.Cell death discovery · 2025Review
- Review
- EnhancerNet: a predictive model of cell identity dynamics through enhancer selection.Development (Cambridge, England) · 2024Article
- Mi-2β promotes immune evasion in melanoma by activating EZH2 methylation.Nature communications · 2024Article
- Early B-Cell Factor 1: An Archetype for a Lineage-Restricted Transcription Factor Linking Development to Disease.Advances in experimental medicine and biology · 2024Review
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- MicroRNA-598 inhibition ameliorates LPS-induced acute lung injury in mice through upregulating Ebf1 expression.Histochemistry and cell biology · 2023Article
- SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023Review
- The Pleiotropy ofInternational journal of molecular sciences · 2022Review
- EBNA2-EBF1 complexes promote MYC expression and metabolic processes driving S-phase progression of Epstein-Barr virus-infected B cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- CHD4 orchestrates the symphony of T and B lymphocytes development and a good mediator in preventing from autoimmune disease.Immunity, inflammation and disease · 2022Review
- Chromodomain helicase DNA-binding 4 (CHD4) regulates early B cell identity and V(D)J recombination.Immunological reviews · 2022Review
- Sentinels of chromatin: chromodomain helicase DNA-binding proteins in development and disease.Genes & development · 2021Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Transcriptionally silent genes are maintained in inaccessible chromatin. Accessibility of these genes requires their modification by chromatin remodeling complexes (CRCs), which are recruited to promoters by sequence-specific DNA-binding proteins. Early B-cell factor (EBF), which is crucial for B-cell lineage specification, reprograms mb-1 (Ig-alpha) promoters by increasing chromatin accessibility and initiating the loss of DNA methylation. In turn, this facilitates promoter activation by Pax5. Here, we investigated the roles of ATP-dependent CRCs in these mechanisms. Fusion of EBF and Pax5 with the ligand-binding domain of ERalpha allowed for 4-hydroxytamoxifen-dependent, synergistic activation of mb-1 transcription in plasmacytoma cells. Knock-down of the SWI/SNF ATPases Brg1 and Brm inhibited transcriptional activation by EBF:ER and Pax5:ER. In contrast, knock-down of the Mi-2/NuRD complex subunit Mi-2beta greatly enhanced chromatin accessibility and mb-1 transcription in response to the activators. The reduction of Mi-2beta also propagated DNA demethylation in response to EBF:ER and Pax5:ER, resulting in fully unmethylated mb-1 promoters. In EBF- or EBF/Pax5-deficient fetal liver cells, both EBF and Pax5 were required for efficient demethylation of mb-1 promoters. Together, our data suggest that Mi-2/NuRD is important for the maintenance of hypermethylated chromatin in B cells. We conclude that SWI/SNF and Mi-2/NuRD function in opposition to enable or limit the reprogramming of genes by EBF and Pax5 during B-cell development.
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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.