Evidence map›Paper›PMID 29125602›Full record

ReviewCell death and differentiation2018

Mechanisms of transcriptional regulation by p53.

Kelly D Sullivan, Matthew D Galbraith, Zdenek Andrysik, Joaquin M Espinosa

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
271citing papers in PubMed, 2 pooled it
17.2field-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

271 citing papers in PubMed, 2 syntheses or guidelines pooled it, 450 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Pooled it
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  13. Unveiling the developmental and tumor-suppressive roles of the p53 variant p53psi.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Unraveling the role ofHemaSphere · 2026
    Review
  15. Article
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  18. Hollow condensates emerge from gelation-induced spinodal decomposition.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Article

211 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

4 authors at 2 institutions in 1 country.

Kelly D SullivanDepartment of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Matthew D GalbraithDepartment of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA.ORCID 0000-0003-0485-3927
Zdenek AndrysikDepartment of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Joaquin M EspinosaDepartment of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA.
University of Colorado Denver · USUniversity of Colorado Boulder · US

Funding

Stress- and Promoter-Specific Mechanisms of Transcritpional Activation by p53R01CA117907 · NCI · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2006 to 2022
$4.4M
NCI NIH HHS R01 CA117907
6 · The paper itself

Abstract

p53 is a transcription factor that suppresses tumor growth through regulation of dozens of target genes with diverse biological functions. The activity of this master transcription factor is inactivated in nearly all tumors, either by mutations in the TP53 locus or by oncogenic events that decrease the activity of the wild-type protein, such as overexpression of the p53 repressor MDM2. However, despite decades of intensive research, our collective understanding of the p53 signaling cascade remains incomplete. In this review, we focus on recent advances in our understanding of mechanisms of p53-dependent transcriptional control as they relate to five key areas: (1) the functionally distinct N-terminal transactivation domains, (2) the diverse regulatory roles of its C-terminal domain, (3) evidence that p53 is solely a direct transcriptional activator, not a direct repressor, (4) the ability of p53 to recognize many of its enhancers across diverse chromatin environments, and (5) mechanisms that modify the p53-dependent transcriptional program in a context-dependent manner.

Indexed as

Transcriptional ActivationAnimalsHumansMiceProtein DomainsRepressor ProteinsTumor Suppressor Protein p53Repressor ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID29125602
PMCPMC5729533
OpenAlexW2767326431

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.