ArticleDevelopment (Cambridge, England)2012
ΔNp63 knockout mice reveal its indispensable role as a master regulator of epithelial development and differentiation.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
203 citing papers in PubMed, 1 synthesis or guideline pooled it, 295 citations in OpenAlex.
- Genome-wide meta-analysis identifies multiple novel associations and ethnic heterogeneity of psoriasis susceptibility.Nature communications · 2015Pooled it
- Lineage master regulator and cancer-selective partner transcription factors rewire 3D genome topology for tumor-specific gene control.Science advances · 2026Article
- Article
- Dynamics, function, and regulation of mammary stem cells in development and disease.Experimental & molecular medicine · 2026Review
- Isoform-specific cofactor recruitment through the intrinsically disordered N-terminus of p63 underlies differential transcriptional activities.bioRxiv : the preprint server for biology · 2026Article
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- Asymmetric histone inheritance regulates olfactory stem cell fates during regeneration.Nature communications · 2026Article
- Unveiling critical signaling pathways in the murine salivary gland and the role of midkine.iScience · 2026Article
- ΔNP63 Defines an Exocrine-committed Subset of Murine Pancreatic Progenitor Cells.Cellular and molecular gastroenterology and hepatology · 2026Article
- Targeting NLRP10 in Atopic Dermatitis: An Emerging Strategy to Modulate Epidermal Cell Death and Barrier Function.International journal of molecular sciences · 2025Review
- Deletion of p63 exon 13 in mice reveals C-terminal isoform-specific functions in epithelial development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- LEADR, a p63 target, dampens interferon signalling in bladder cancer.Cell death discovery · 2025Article
- Review
- TAp63γ is the primary isoform of TP63 for tumor suppression but not development.Cell death discovery · 2025Article
- Uterine organoids reveal insights into epithelial specification and plasticity in development and disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- TAp73 and ΔTAp73 isoforms show cell-type specific distributions and alterations in cancer.Scientific reports · 2024Article
- BRD4 sustains p63 transcriptional program in keratinocytes.Biology direct · 2024Article
- Overview of chromatin regulatory processes during surface ectodermal development and homeostasis.Developmental biology · 2024Review
143 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
The transcription factor p63 is important in the development of the skin as p63-null mice exhibit striking defects in embryonic epidermal morphogenesis. Understanding the mechanisms that underlie this phenotype is complicated by the existence of multiple p63 isoforms, including TAp63 and ΔNp63. To investigate the role of ΔNp63 in epidermal morphogenesis we generated ΔNp63 knock-in mice in which the ΔNp63-specific exon is replaced by GFP. Homozygous ΔNp63(gfp/gfp) animals exhibit severe developmental anomalies including truncated forelimbs and the absence of hind limbs, largely phenocopying existing knockouts in which all p63 isoforms are deleted. ΔNp63-null animals show a poorly developed stratified epidermis comprising isolated clusters of disorganized epithelial cells. Despite the failure to develop a mature stratified epidermis, the patches of ΔNp63-null keratinocytes are able to stratify and undergo a program of terminal differentiation. However, we observe premature expression of markers associated with terminal differentiation, which is unique to ΔNp63-null animals and not evident in the skin of mice lacking all p63 isoforms. We posit that the dysregulated and accelerated keratinocyte differentiation phenotype is driven by significant alterations in the expression of key components of the Notch signaling pathway, some of which are direct transcriptional targets of ΔNp63 as demonstrated by ChIP experiments. The analysis of ΔNp63(gfp/gfp) knockout mice reaffirms the indispensable role of the ΔN isoform of p63 in epithelial biology and confirms that ΔNp63-null keratinocytes are capable of committing to an epidermal cell lineage, but are likely to suffer from diminished renewal capacity and an altered differentiation fate.
Indexed as
Identifiers
What OpenQuestion holds
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.