Evidence map›Paper›PMID 24037342›Full record

ArticleThe Journal of investigative dermatology2014

Dominant effects of Δ40p53 on p53 function and melanoma cell fate.

Rie Takahashi, Svetomir N Markovic, Heidi J Scrable

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. A Novel Mechanism of the p53 Isoform Δ40p53α in Regulating Collagen III Expression in TGFβ1-Induced LX-2 Human Hepatic Stellate Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  6. Review
  7. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Δ40p53 isoform up-regulates netrin-1/UNC5B expression and potentiates netrin-1 pro-oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article
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

3 authors at 2 institutions in 1 country.

Rie TakahashiMedical Scientist Training Program, Mayo Clinic, Rochester, Minnesota, USA; Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA; Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
Svetomir N MarkovicInternal Medicine/Division of Hematology, Mayo Clinic, Rochester, Minnesota, USA; Oncology/Division of Medical Oncology, Mayo Clinic, Rochester, Minnesota, USA; Immunology, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: Markovic.Svetomir@mayo.edu.
Heidi J ScrableBiochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA; Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA; Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
Mayo Clinic in Florida · USMayo Clinic · US

Funding

The Sir2-p53-IGF Link in Mammalian Life-Span ControlR01AG026094 · NIA · UNIVERSITY OF VIRGINIA · PI CHINI, EDUARDO N · 2006 to 2016
$3.8M
NIA NIH HHS R01 AG026094
6 · The paper itself

Abstract

The TP53 gene encodes 12 distinct isoforms, some of which can alter p53 activity in the absence of genomic alteration. Endogenous p53 isoforms have been identified in cancers; however, the function of these isoforms remains unclear. In melanoma, the frequency of TP53 mutations is relatively low compared with other cancers, suggesting that these isoforms may have a larger role in regulating TP53 activity. We hypothesized that p53 function and therefore cell fate might be altered by the presence of Δ40p53, an embryonic isoform missing the first 40 N-terminal amino acids of the full-length protein including the transactivation and Mdm2-binding domains. To test this hypothesis, we transduced tumor and normal cells with a lentivirus encoding Δ40p53. We found that exogenous Δ40p53 caused apoptosis and increased the levels of endogenous, activated p53 in both cancerous and non-cancerous cells, which led to significant levels of cell death, particularly in cancer cells. Activated p53 molecules formed nuclear heterotetramers with Δ40p53 and altered downstream p53 transcription target levels including p53-induced protein with death domain and cyclin-dependent kinase inhibitor, p21. Δ40p53 altered the promoter occupancy of these downstream p53 target genes in such a way that it shifted cell fate toward apoptosis and away from cell cycle arrest. We show that tumor suppression by p53 can occur via an alternate route that relies on its interaction with Δ40p53.

Indexed as

AnimalsApoptosisBrain NeoplasmsCell Cycle CheckpointsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21Death Domain Receptor Signaling Adaptor ProteinsFibroblastsGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGlioblastomaHumansMelanocytesMelanomaMicePromoter Regions, GeneticCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Death Domain Receptor Signaling Adaptor ProteinsPIDD1 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24037342
PMCPMC3945389
OpenAlexW2066817359

What OpenQuestion holds

Textmetadata
LicenceTDM
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.