Evidence map›Paper›PMID 20679336›Full record

ReviewCold Spring Harbor perspectives in biology2010

Transcriptional regulation by p53.

Rachel Beckerman, Carol Prives

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 342 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
342citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

342 citing papers in PubMed, 2 syntheses or guidelines pooled it, 577 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025
    Review
  18. Article
  19. Review
  20. Article

282 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

2 authors at 1 institution in 1 country.

Rachel BeckermanDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA.
Carol Prives
Columbia University · US

Funding

Scientific ReagentsP01CA087497 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 2000 to 2021
$35.4M
PROPERTIES AND REGULATION OF P53 IN TUMOR CELLSR01CA077742 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1999 to 2014
$3.8M
NCI NIH HHS CA77742NCI NIH HHS CA87497NCI NIH HHS P01 CA087497NCI NIH HHS R01 CA077742
6 · The paper itself

Abstract

Inactivation of p53 is critical for the formation of most tumors. Illumination of the key function(s) of p53 protein in protecting cells from becoming cancerous is therefore a worthy goal. Arguably p53's most important function is to act as a transcription factor that directly regulates perhaps several hundred of the cell's RNA polymerase II (RNAP II)-transcribed genes, and indirectly regulates thousands of others. Indeed p53 is the most well studied mammalian transcription factor. The p53 tetramer binds to its response element where it can recruit diverse transcriptional coregulators such as histone modifying enzymes, chromatin remodeling factors, subunits of the mediator complex, and components of general transcription machinery and preinitiation complex (PIC) to modulate RNAPII activity at target loci (Laptenko and Prives 2006). The p53 transcriptional program is regulated in a stimulus-specific fashion (Murray-Zmijewski et al. 2008; Vousden and Prives 2009), whereby distinct subsets of p53 target genes are induced in response to different p53-activating agents, likely allowing cells to tailor their response to different types of stress. How p53 is able to discriminate between these different loci is the subject of intense research. Here, we describe key aspects of the fundamentals of p53-mediated transcriptional regulation and target gene promoter selectivity.

Indexed as

Gene Expression RegulationGenes, p53Transcription, GeneticAnimalsChromatinGene Expression Regulation, NeoplasticHumansModels, BiologicalNeoplasmsPromoter Regions, GeneticResponse ElementsRNA Polymerase IISignal TransductionTumor Suppressor Protein p53ChromatinRNA Polymerase IITumor Suppressor Protein p53

Identifiers

PMID20679336
PMCPMC2908772
OpenAlexW2138566050

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.