ArticleiScience2023
GRHL2 and AP2a coordinate early surface ectoderm lineage commitment during development.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
- KMT2C and KMT2D amplify GRHL2-driven enhancer activation.bioRxiv : the preprint server for biology · 2026Article
- YAP-TEAD regulates the super-enhancer network to control early surface ectoderm commitment.Nucleic acids research · 2026Article
- Haploinsufficiency of GRHL2 is associated with orofacial clefting in humans.Human molecular genetics · 2025Article
- FOXO4-SP6 axis controls surface epithelium commitment by mediating epigenomic remodeling.Stem cell reports · 2025Article
- C1-linker region of PARG1 RhoGAP promotes the catalytic recognition fold of RhoA substrate.PloS one · 2025Article
- AP-2α/AP-2β Transcription Factors Are Key Regulators of Epidermal Homeostasis.The Journal of investigative dermatology · 2024Article
- In vitro induction of patterned branchial arch-like aggregate from human pluripotent stem cells.Nature communications · 2024Article
- AP-2α/AP-2β transcription factors are key regulators of epidermal homeostasis.bioRxiv : the preprint server for biology · 2023Article
- Rare variants found in multiplex families with orofacial clefts: Does expanding the phenotype make a difference?American journal of medical genetics. Part A · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Ectodermal dysplasias including skin abnormalities and cleft lip/palate result from improper surface ectoderm (SE) patterning. However, the connection between SE gene regulatory networks and disease remains poorly understood. Here, we dissect human SE differentiation with multiomics and establish GRHL2 as a key mediator of early SE commitment, which acts by skewing cell fate away from the neural lineage. GRHL2 and master SE regulator AP2a balance early cell fate output, with GRHL2 facilitating AP2a binding to SE loci. In turn, AP2a restricts GRHL2 DNA binding away from
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Registered trials
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.