Evidence map›Paper›PMID 10380877›Full record

ArticleOncogene1999

Mutant p53 proteins stimulate spontaneous and radiation-induced intrachromosomal homologous recombination independently of the alteration of the transactivation activity and of the G1 checkpoint.

Y Saintigny, D Rouillard, B Chaput, T Soussi, B S Lopez

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
  2. When PIPFrontiers in cell and developmental biology · 2022
    Review
  3. Drugging in the absence of p53.Journal of molecular cell biology · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016
    Review
  9. Review
  10. Review
  11. Article
  12. Genetically defined subsets of human pancreatic cancer show unique in vitro chemosensitivity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Differential cellular responses to prolonged LDR-IR in MLH1-proficient and MLH1-deficient colorectal cancer HCT116 cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  19. Article
  20. Review
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

5 authors at 3 institutions in 1 country.

Y SaintignyUnité Mixte de Recherches CEA-CNRS 217, CEA, DSV, DRR, Fontenay aux Roses, France.
D Rouillard
B Chaput
T Soussi
B S Lopez
Centre National de la Recherche Scientifique · FRInstitut Curie · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We report here a systematic analysis of the effects of different p53 mutations on both spontaneous and radiation-stimulated homologous recombination in mouse L cells. In order to monitor different recombination pathways, we used both direct and inverted repeat recombination substrates. In each line bearing one of these substrates, we expressed p53 proteins mutated at positions: 175, 248 or 273. p53 mutations leading to an increased spontaneous recombination rate also stimulate radiation-induced recombination. The effect on recombination may be partially related to the conformation of the p53 protein. Moreover, p53 mutations act on recombination between direct repeats as well as between inverted repeats indicating that strand invasion mechanisms are stimulated. Although all of the p53 mutations affect the p53 transactivation activity measured on the WAF1 and MDM2 gene promoters, no correlation between the transactivation activity and the extent of homologous recombination can be drawn. Finally, some p53 mutations do not affect the G1 arrest after radiation but stimulate radiation-induced recombination. These results show that the role of p53 on transactivation and G1 cell cycle checkpoint is separable from its involvement in homologous recombination. A direct participation of p53 in the recombination mechanism itself is discussed.

Indexed as

G1 PhaseMutationNuclear ProteinsRecombination, GeneticTranscriptional ActivationAnimalsCell DeathCell LineCyclin-Dependent Kinase Inhibitor p21CyclinsDNA, Single-StrandedGamma RaysMicePromoter Regions, GeneticProtein ConformationProto-Oncogene ProteinsCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21CyclinsDNA, Single-StrandedMdm2 protein, mouseNuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID10380877
OpenAlexW2323231231

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.