Evidence map›Paper›PMID 31216312›Full record

ArticlePloS one2019

p73 regulates epidermal wound healing and induced keratinocyte programming.

J Scott Beeler, Clayton B Marshall, Paula I Gonzalez-Ericsson, Timothy M Shaver, Gabriela L Santos Guasch, Spencer T Lea, Kimberly N Johnson, Hailing Jin, Bryan J Venters, Melinda E Sanders and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Generation of theInternational journal of molecular sciences · 2025
    Article
  3. Article
  4. Review
  5. Loss of p73 Expression Contributes to Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. MDM2, MDMX, and p73 regulate cell-cycle progression in the absence of wild-type p53.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Oh, the Mutations You'll Acquire! A Systematic Overview of Cutaneous Squamous Cell Carcinoma.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Review
  19. Article
  20. Review
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

11 authors at 2 institutions in 1 country.

J Scott BeelerDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.ORCID 0000-0002-1829-1972
Clayton B MarshallDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.
Paula I Gonzalez-EricssonVanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Timothy M ShaverDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.
Gabriela L Santos GuaschDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.
Spencer T LeaDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.
Kimberly N JohnsonVanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Hailing JinVanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Bryan J VentersVanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Melinda E SandersVanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Jennifer A PietenpolDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.ORCID 0000-0001-6268-6798
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
P53 SIGNALING AND CELLULAR RESPONSE AFTER STRESSR01CA070856 · NCI · VANDERBILT UNIVERSITY · PI PIETENPOL, JENNIFER A · 1997 to 2010
$3.8M
p63 Signaling in Epithelial Cell Growth and CancerR01CA105436 · NCI · VANDERBILT UNIVERSITY · PI PIETENPOL, JENNIFER A · 2004 to 2014
$3.1M
Leica Bond RXS10OD023475 · OD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOYD, KELLI L. · 2018 to 2018
$213k
NCI NIH HHS P30 CA068485NCI NIH HHS P50 CA098131NCI NIH HHS R01 CA070856NCI NIH HHS R01 CA105436NIGMS NIH HHS R25 GM062459NIGMS NIH HHS T32 GM007347NIH HHS S10 OD023475
6 · The paper itself

Abstract

p63 is a transcriptional regulator of ectodermal development that is required for basal cell proliferation and stem cell maintenance. p73 is a closely related p53 family member that is expressed in select p63-positive basal cells and can heterodimerize with p63. p73-/- mice lack multiciliated cells and have reduced numbers of basal epithelial cells in select tissues; however, the role of p73 in basal epithelial cells is unknown. Herein, we show that p73-deficient mice exhibit delayed wound healing despite morphologically normal-appearing skin. The delay in wound healing is accompanied by decreased proliferation and increased levels of biomarkers of the DNA damage response in basal keratinocytes at the epidermal wound edge. In wild-type mice, this same cell population exhibited increased p73 expression after wounding. Analyzing single-cell transcriptomic data, we found that p73 was expressed by epidermal and hair follicle stem cells, cell types required for wound healing. Moreover, we discovered that p73 isoforms expressed in the skin (ΔNp73) enhance p63-mediated expression of keratinocyte genes during cellular reprogramming from a mesenchymal to basal keratinocyte-like cell. We identified a set of 44 genes directly or indirectly regulated by ΔNp73 that are involved in skin development, cell junctions, cornification, proliferation, and wound healing. Our results establish a role for p73 in cutaneous wound healing through regulation of basal keratinocyte function.

Indexed as

AnimalsCell ProliferationDNA DamageEctodermEpithelial CellsGene Expression Regulation, DevelopmentalHair FollicleHumansKeratinocytesMiceMice, KnockoutSingle-Cell AnalysisSkinStem Cell NicheTrans-ActivatorsTumor Protein p73Trans-ActivatorsTrp63 protein, mouseTrp73 protein, mouseTumor Protein p73

Identifiers

PMID31216312
PMCPMC6583996
OpenAlexW2952967374

What OpenQuestion holds

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LicenceCC BY
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.