Evidence map›Paper›PMID 27754743›Full record

ArticleCell cycle (Georgetown, Tex.)2016

p53 oligomerization status modulates cell fate decisions between growth, arrest and apoptosis.

Nicholas W Fischer, Aaron Prodeus, David Malkin, Jean Gariépy

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  5. Article
  6. Emerging insights into ethnic-specific TP53 germline variants.Journal of the National Cancer Institute · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. CRISPR-based mFrontiers in cell and developmental biology · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  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

4 authors at 3 institutions in 1 country.

Nicholas W Fischera Department of Medical Biophysics , University of Toronto , Toronto , Ontario , Canada.
Aaron Prodeusa Department of Medical Biophysics , University of Toronto , Toronto , Ontario , Canada.
David Malkina Department of Medical Biophysics , University of Toronto , Toronto , Ontario , Canada.
Jean Gariépya Department of Medical Biophysics , University of Toronto , Toronto , Ontario , Canada.
University of Toronto · CASunnybrook Health Science Centre · CASunnybrook Research Institute

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the oligomerization domain of p53 are genetically linked to cancer susceptibility in Li-Fraumeni Syndrome. These mutations typically alter the oligomeric state of p53 and impair its transcriptional activity. Activation of p53 through tetramerization is required for its tumor suppressive function by inducing transcriptional programs that lead to cell fate decisions such as cell cycle arrest or apoptosis. How p53 chooses between these cell fate outcomes remains unclear. Here, we use 5 oligomeric variants of p53, including 2 novel p53 constructs, that yield either monomeric, dimeric or tetrameric forms of p53 and demonstrate that they induce distinct cellular activities and gene expression profiles that lead to different cell fate outcomes. We report that dimeric p53 variants are cytostatic and can arrest cell growth, but lack the ability to trigger apoptosis in p53-null cells. In contrast, p53 tetramers induce rapid apoptosis and cell growth arrest, while a monomeric variant is functionally inactive, supporting cell growth. In particular, the expression of pro-arrest CDKN1A and pro-apoptotic P53AIP1 genes are important cell fate determinants that are differentially regulated by the oligomeric state of p53. This study suggests that the most abundant oligomeric species of p53 present in resting cells, namely p53 dimers, neither promote cell growth or cell death and that shifting the oligomeric state equilibrium of p53 in cells toward monomers or tetramers is a key parameter in p53-based cell fate decisions.

Indexed as

ApoptosisCell Cycle CheckpointsCell LineageProtein MultimerizationAmino Acid SequenceCell Line, TumorCell ProliferationGene Expression RegulationHumansTranscription, GeneticTumor Suppressor Protein p53Tumor Suppressor Protein p53apoptosiscell cycle arrestcell fateoligomerizationp53tumor suppressor

Identifiers

PMID27754743
PMCPMC5176156
OpenAlexW2534096574

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.