ArticleAmerican journal of human genetics2024
ARID1A-BAF coordinates ZIC2 genomic occupancy for epithelial-to-mesenchymal transition in cranial neural crest specification.
Article in American journal of human genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Dual role of ZIC2 during neural induction: from priming transcription factor to enhancer activator.Nucleic acids research · 2026Article
- Cell fate specification during respiratory development requires ARID1A-containing canonical BAF complex activity.Nature communications · 2026Article
- Lung cancer-enriched p53 mutants occupy canonical p53 target genes without activating transcription, revealing a distinct loss-of-function behavior.bioRxiv : the preprint server for biology · 2026Article
- Neural crest induction requires SALL4-mediated BAF recruitment to lineage specific enhancers.Development (Cambridge, England) · 2025Article
- Hominoid-specific transposable elements reshaped neural crest migration in craniofacial development.Molecular systems biology · 2025Article
- A chemical epigenetic tool to probe site-specific DNA-binding protein complexes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The NuRD component CHD3 promotes BMP signalling during cranial neural crest cell specification.EMBO reports · 2025Article
- Wnt5a and Notum influence the temporal dynamics of cartilaginous mesenchymal condensations in developing trachea.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
The BAF chromatin remodeler regulates lineage commitment including cranial neural crest cell (CNCC) specification. Variants in BAF subunits cause Coffin-Siris syndrome (CSS), a congenital disorder characterized by coarse craniofacial features and intellectual disability. Approximately 50% of individuals with CSS harbor variants in one of the mutually exclusive BAF subunits, ARID1A/ARID1B. While Arid1a deletion in mouse neural crest causes severe craniofacial phenotypes, little is known about the role of ARID1A in CNCC specification. Using CSS-patient-derived ARID1A
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Registered trials
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