ArticleNucleic acids research2021
BACH1 recruits NANOG and histone H3 lysine 4 methyltransferase MLL/SET1 complexes to regulate enhancer-promoter activity and maintains pluripotency.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- A spinal USP7-Bach1 positive feedback loop drives NOX4-mediated ferroptosis in neuropathic pain.Redox biology · 2026Article
- A positive feedback loop between BACH1 and IL-1β promotes the progression of HPV-negative head and neck squamous cell carcinoma.Cell communication and signaling : CCS · 2026Article
- Bromodomain-Driven Regulation of Stem Cells: A Potential Target for Cancer Therapeutic Intervention.Stem cell reviews and reports · 2026Review
- WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.Nature communications · 2026Article
- Monitoring rapid degradation of NANOG reveals UTP15 maintains pluripotency by regulating nascent transcripts.Nature communications · 2025Article
- THBru ameliorates atherosclerosis by inhibiting endothelial ferroptosisActa pharmaceutica Sinica. B · 2025Article
- Targeting BACH1 by HPPE inhibits the Wnt/β-catenin pathway and malignant phenotype in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2025Article
- Super-Enhancer Target Gene CBP/p300-Interacting Transactivator With Glu/Asp-Rich C-Terminal Domain, 2 Cooperates With Transcription Factor Forkhead Box J3 to Inhibit Pulmonary Vascular Remodeling.Cell proliferation · 2025Article
- BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells.Stem cell research & therapy · 2025Article
- Let-7 restrains an epigenetic circuit in AT2 cells to prevent fibrogenic intermediates in pulmonary fibrosis.Nature communications · 2025Article
- BACH1 deficiency improves placental angiogenesis via SLC25A51-mediated mitochondrial NADMolecular medicine (Cambridge, Mass.) · 2025Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Effects of Exogenous Regulation of PPARγ on Ovine Oocyte Maturation and Embryonic Development In Vitro.Veterinary sciences · 2024Article
- LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B.Journal of experimental & clinical cancer research : CR · 2024Article
- Super-enhancers: drivers of cells' identities and cells' debacles.Epigenomics · 2024Review
- Kaposi's sarcoma-associated herpesvirus terminal repeat regulates inducible lytic gene promoters.Journal of virology · 2024Article
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- BACH1 controls hepatic insulin signaling and glucose homeostasis in mice.Nature communications · 2023Article
- RBBP4 is an epigenetic barrier for the induced transition of pluripotent stem cells into totipotent 2C-like cells.Nucleic acids research · 2023Article
- BACH1 deficiency prevents neointima formation and maintains the differentiated phenotype of vascular smooth muscle cells by regulating chromatin accessibility.Nucleic acids research · 2023Article
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance of stem-cell identity requires proper regulation of enhancer activity. Both transcription factors OCT4/SOX2/NANOG and histone methyltransferase complexes MLL/SET1 were shown to regulate enhancer activity, but how they are regulated in embryonic stem cells (ESCs) remains further studies. Here, we report a transcription factor BACH1, which directly interacts with OCT4/SOX2/NANOG (OSN) and MLL/SET1 methyltransferase complexes and maintains pluripotency in mouse ESCs (mESCs). BTB domain and bZIP domain of BACH1 are required for these interactions and pluripotency maintenance. Loss of BACH1 reduced the interaction between NANOG and MLL1/SET1 complexes, and decreased their occupancy on chromatin, and further decreased H3 lysine 4 trimethylation (H3K4me3) level on gene promoters and (super-) enhancers, leading to decreased enhancer activity and transcription activity, especially on stemness-related genes. Moreover, BACH1 recruited NANOG through chromatin looping and regulated remote NANOG binding, fine-tuning enhancer-promoter activity and gene expression. Collectively, these observations suggest that BACH1 maintains pluripotency in ESCs by recruiting NANOG and MLL/SET1 complexes to chromatin and maintaining the trimethylated state of H3K4 and enhancer-promoter activity, especially on stemness-related genes.
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