Evidence map›Paper›PMID 22274697›Full record

ArticleDevelopment (Cambridge, England)2012

ΔNp63 knockout mice reveal its indispensable role as a master regulator of epithelial development and differentiation.

Rose-Anne Romano, Kirsten Smalley, Caitlin Magraw, Vanida Ann Serna, Takeshi Kurita, Srikala Raghavan, Satrajit Sinha

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 1 pooled it
14.4field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

203 citing papers in PubMed, 1 synthesis or guideline pooled it, 295 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. ΔNP63 Defines an Exocrine-committed Subset of Murine Pancreatic Progenitor Cells.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  10. Review
  11. 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 · 2025
    Article
  12. 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 · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. 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 · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Review

143 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Rose-Anne RomanoDepartment of Biochemistry, Center for Excellence in Bioinformatics and Life Sciences, State University of New York at Buffalo, NY 14203, USA. rromano2@buffalo.edu
Kirsten Smalley
Caitlin Magraw
Vanida Ann Serna
Takeshi Kurita
Srikala Raghavan
Satrajit Sinha
University at Buffalo, State University of New York · USColumbia University · USNorthwestern University · US

Funding

Molecular Etiology of Cervicovaginal Adenosis by in Utero Hormone ExposureR01CA154358 · NCI · OHIO STATE UNIVERSITY · PI KURITA, TAKESHI · 2010 to 2014
$1.5M
Transcriptional control of epidermal differentiationR01AR049238 · NIAMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SINHA, SATRAJIT · 2004 to 2008
$1.4M
NCI NIH HHS R01 CA154358NCI NIH HHS R01CA154358NIAMS NIH HHS R01 AR049238NIAMS NIH HHS R01AR049238
6 · The paper itself

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

Mice, KnockoutAnimalsBiomarkersCell DifferentiationEmbryo, MammalianEpidermisEpithelial CellsEpitheliumExtracellular MatrixHumansIntercellular JunctionsKeratinocytesMiceMorphogenesisPhosphoproteinsProtein IsoformsBiomarkersPhosphoproteinsProtein IsoformsReceptors, NotchTrans-ActivatorsTrp63 protein, mouse

Identifiers

PMID22274697
PMCPMC3265062
OpenAlexW1977436879

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.