ArticleProceedings of the National Academy of Sciences of the United States of America2008
ES cell pluripotency and germ-layer formation require the SWI/SNF chromatin remodeling component BAF250a.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 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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Who cites it
218 citing papers in PubMed, 343 citations in OpenAlex.
- BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- Arginine methylation of BAF155 regulates interactions with RNA processing machinery.bioRxiv : the preprint server for biology · 2026Article
- ISWI remodeler facilitates cBAF genomic binding to drive cell fate transition.bioRxiv : the preprint server for biology · 2026Article
- Cell fate specification during respiratory development requires ARID1A-containing canonical BAF complex activity.Nature communications · 2026Article
- Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.Nature communications · 2026Article
- H3K9me2 is a determinant for the mitosis-to-meiosis transition in female germ cells.Cell death & disease · 2026Article
- How ATP-Dependent Chromatin Remodeling Complexes Regulate Vertebrate Embryonic Development.International journal of molecular sciences · 2026Review
- Article
- Arid1a Deficiency Drives Aristolochic Acid-Induced Liver Tumorigenesis through Ctnnb1 Mutation and Defective Nucleotide Excision Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- BRG1 (SMARCA4) Status Dictates the Response to EGFR Inhibitors in Wild-Type EGFR Non-Small Cell Lung Cancer.Cancers · 2025Article
- Synovial sarcoma reprograms transcription by GBAF activation of polycomb targets and loss of CBAF enhancers.Nature communications · 2025Article
- Epigenetic control of cell identities from epiblast to gastrulation.The FEBS journal · 2025Review
- Disruption of ARID1B Recruitment to the Nuclear Pore Complex as a New Anticancer Therapeutic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ARID1A: gene, protein, and function in endometrial cancer.Oncogene · 2025Review
- Systematic genetic perturbation reveals principles underpinning robustness of the epigenetic regulatory network.Nucleic acids research · 2025Article
- Loss of ARID1A accelerates prostate tumourigenesis with a proliferative collagen-poor phenotype through co-operation with AP1 subunit cFos.British journal of cancer · 2025Article
- Arid1a-dependent canonical BAF complex suppresses inflammatory programs to drive efficient germinal center B cell responses.Nature immunology · 2024Article
- Article
- Microglia homeostasis mediated by epigenetic ARID1A regulates neural progenitor cells response and leads to autism-like behaviors.Molecular psychiatry · 2024Article
- Smad4 restricts injury-provoked biliary proliferation and carcinogenesis.Disease models & mechanisms · 2024Article
158 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
ATP-dependent chromatin remodeling complexes are a notable group of epigenetic modifiers that use the energy of ATP hydrolysis to change the structure of chromatin, thereby altering its accessibility to nuclear factors. BAF250a (ARID1a) is a unique and defining subunit of the BAF chromatin remodeling complex with the potential to facilitate chromosome alterations critical during development. Our studies show that ablation of BAF250a in early mouse embryos results in developmental arrest (about embryonic day 6.5) and absence of the mesodermal layer, indicating its critical role in early germ-layer formation. Moreover, BAF250a deficiency compromises ES cell pluripotency, severely inhibits self-renewal, and promotes differentiation into primitive endoderm-like cells under normal feeder-free culture conditions. Interestingly, this phenotype can be partially rescued by the presence of embryonic fibroblast cells. DNA microarray, immunostaining, and RNA analyses revealed that BAF250a-mediated chromatin remodeling contributes to the proper expression of numerous genes involved in ES cell self-renewal, including Sox2, Utf1, and Oct4. Furthermore, the pluripotency defects in BAF250a mutant ES cells appear to be cell lineage-specific. For example, embryoid body-based analyses demonstrated that BAF250a-ablated stem cells are defective in differentiating into fully functional mesoderm-derived cardiomyocytes and adipocytes but are capable of differentiating into ectoderm-derived neurons. Our results suggest that BAF250a is a key component of the gene regulatory machinery in ES cells controlling self-renewal, differentiation, and cell lineage decisions.
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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.