Evidence map›Paper›PMID 25486564›Full record

ArticleCell cycle (Georgetown, Tex.)2014

The transcription factor p53: not a repressor, solely an activator.

Martin Fischer, Lydia Steiner, Kurt Engeland

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 3 pooled it
4.9field-weighted citation impact, top 4% 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

110 citing papers in PubMed, 3 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Review
  7. Article
  8. The Tumor Suppressor p53 Downregulates p107 (International journal of molecular sciences · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

50 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

3 authors at 2 institutions in 2 countries.

Martin Fischera Molecular Oncology; Medical School ; University of Leipzig ; Leipzig , Germany.
Lydia Steiner
Kurt Engeland
Leipzig University · DEMolecular Oncology (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The predominant function of the tumor suppressor p53 is transcriptional regulation. It is generally accepted that p53-dependent transcriptional activation occurs by binding to a specific recognition site in promoters of target genes. Additionally, several models for p53-dependent transcriptional repression have been postulated. Here, we evaluate these models based on a computational meta-analysis of genome-wide data. Surprisingly, several major models of p53-dependent gene regulation are implausible. Meta-analysis of large-scale data is unable to confirm reports on directly repressed p53 target genes and falsifies models of direct repression. This notion is supported by experimental re-analysis of representative genes reported as directly repressed by p53. Therefore, p53 is not a direct repressor of transcription, but solely activates its target genes. Moreover, models based on interference of p53 with activating transcription factors as well as models based on the function of ncRNAs are also not supported by the meta-analysis. As an alternative to models of direct repression, the meta-analysis leads to the conclusion that p53 represses transcription indirectly by activation of the p53-p21-DREAM/RB pathway.

Indexed as

Binding SitesChromatin ImmunoprecipitationCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsHCT116 CellsHumansMeta-Analysis as TopicPromoter Regions, GeneticProtein BindingReal-Time Polymerase Chain ReactionRepressor ProteinsRetinoblastoma ProteinRNA, MessengerRNA, UntranslatedSignal TransductionTranscriptional ActivationCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsRepressor ProteinsRetinoblastoma ProteinRNA, MessengerRNA, UntranslatedTumor Suppressor Protein p53CDE, cell cycle-dependent elementcdk, cyclin-dependent kinaseCDKN1AChIP, chromatin immunoprecipitationCHR, cell cycle genes homology regionDREAM complexDREAM, DP, RB-like, E2F4, and MuvB complexE2F/RB complexgenome-wide meta-analysisHPV, human papilloma virusNF-Y, Nuclear factor Yp53

Identifiers

PMID25486564
PMCPMC4612452
OpenAlexW2074447982

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.