ArticleNucleic acids research2012
Genome-wide analysis of p63 binding sites identifies AP-2 factors as co-regulators of epidermal differentiation.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.
What it found
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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
72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.
- Genome-wide meta-analysis implicates mediators of hair follicle development and morphogenesis in risk for severe acne.Nature communications · 2018Pooled it
- Tooth agenesis and orofacial clefting: genetic brothers in arms?Human genetics · 2016Pooled it
- Lineage master regulator and cancer-selective partner transcription factors rewire 3D genome topology for tumor-specific gene control.Science advances · 2026Article
- Novel variants ofFrontiers in genetics · 2026Article
- Functional Validation of Noncoding Variants Associated With Nonsyndromic Orofacial Cleft.Human mutation · 2025Review
- Crosstalk between paralogs and isoforms influences p63-dependent regulatory element activity.Nucleic acids research · 2024Article
- ΔNp63α promotes radioresistance in esophageal squamous cell carcinoma through the PLEC-KEAP1-NRF2 feedback loop.Cell death & disease · 2024Article
- Context dependent activity of p63-bound gene regulatory elements.bioRxiv : the preprint server for biology · 2024Article
- The urothelial gene regulatory network: understanding biology to improve bladder cancer management.Oncogene · 2024Review
- An intronic SNP affects skeletal muscle development by regulating the expression ofFrontiers in veterinary science · 2024Article
- Direct Lineage Reprogramming for Induced Keratinocyte Stem Cells: A Potential Approach for Skin Repair.Stem cells translational medicine · 2023Review
- Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.Cell death & disease · 2023Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- The TΑp63/BCL2 axis represents a novel mechanism of clinical aggressiveness in chronic lymphocytic leukemia.Blood advances · 2022Article
- Mouse models in palate development and orofacial cleft research: Understanding the crucial role and regulation of epithelial integrity in facial and palate morphogenesis.Current topics in developmental biology · 2022Article
- Family based and case-control designs reveal an association of TFAP2A in nonsyndromic cleft lip only among Vietnamese population.Molecular genetics & genomic medicine · 2021Article
- Interaction of the NRF2 and p63 transcription factors promotes keratinocyte proliferation in the epidermis.Nucleic acids research · 2021Article
- Isoform-Specific Roles of Mutant p63 in Human Diseases.Cancers · 2021Review
- p63 and p53: Collaborative Partners or Dueling Rivals?Frontiers in cell and developmental biology · 2021Review
- Article
12 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
14 authors at 3 institutions in 1 country.
Funding
Abstract
The p63 transcription factor (TP63) is critical in development, growth and differentiation of stratifying epithelia. This is highlighted by the severity of congenital abnormalities caused by TP63 mutations in humans, the dramatic phenotypes in knockout mice and de-regulation of TP63 expression in neoplasia altering the tumour suppressive roles of the TP53 family. In order to define the normal role played by TP63 and provide the basis for better understanding how this network is perturbed in disease, we used chromatin immunoprecipitation combined with massively parallel sequencing (ChIP-seq) to identify >7500 high-confidence TP63-binding regions across the entire genome, in primary human neonatal foreskin keratinocytes (HFKs). Using integrative strategies, we demonstrate that only a subset of these sites are bound by TP53 in response to DNA damage. We identify a role for TP63 in transcriptional regulation of multiple genes genetically linked to cleft palate and identify AP-2alpha (TFAP2A) as a co-regulator of a subset of these genes. We further demonstrate that AP-2gamma (TFAP2C) can bind a subset of these regions and that acute depletion of either TFAP2A or TFAP2C alone is sufficient to reduce terminal differentiation of organotypic epidermal skin equivalents, indicating overlapping physiological functions with TP63.
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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.