ArticleOncogene2002
Wild-type p53 inhibits replication-associated homologous recombination.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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.
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Who cites it
25 citing papers in PubMed, 60 citations in OpenAlex.
- RNA-Based Classification of Homologous Recombination Deficiency in Racially Diverse Patients with Breast Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022Article
- The C-terminus of Gain-of-Function Mutant p53 R273H Is Required for Association with PARP1 and Poly-ADP-Ribose.Molecular cancer research : MCR · 2022Article
- Differences in genetics and microenvironment of lung adenocarcinoma patients with or without TP53 mutation.BMC pulmonary medicine · 2021Article
- Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- Functional relationship between p53 and RUNX proteins.Journal of molecular cell biology · 2019Review
- Drugging in the absence of p53.Journal of molecular cell biology · 2019Review
- p53 orchestrates DNA replication restart homeostasis by suppressing mutagenic RAD52 and POLθ pathways.eLife · 2018Article
- Targeting Cyclin-Dependent Kinases for Treatment of Gynecologic Cancers.Frontiers in oncology · 2018Review
- Homologous recombination defects and how they affect replication fork maintenance.AIMS genetics · 2018Review
- Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.Oncogene · 2016Article
- Chromosome instability and deregulated proliferation: an unavoidable duo.Cellular and molecular life sciences : CMLS · 2012Review
- p53 null fluorescent yellow direct repeat (FYDR) mice have normal levels of homologous recombination.DNA repair · 2011Article
- Reduced level of ribonucleotide reductase R2 subunits increases dependence on homologous recombination repair of cisplatin-induced DNA damage.Molecular pharmacology · 2011Article
- Article
- Reduction of gene repair by selenomethionine with the use of single-stranded oligonucleotides.BMC molecular biology · 2007Article
- Suppression of replication fork progression in low-dose-specific p53-dependent S-phase DNA damage checkpoint.Oncogene · 2006Article
- Threshold effects of nitric oxide-induced toxicity and cellular responses in wild-type and p53-null human lymphoblastoid cells.Chemical research in toxicology · 2006Article
- Poly(ADP-RIBOSE) polymerase-1 (Parp-1) antagonizes topoisomerase I-dependent recombination stimulation by P53.Nucleic acids research · 2006Article
- Differences in the association of p53 phosphorylated on serine 15 and key enzymes of homologous recombination.Oncogene · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammalian cells homologous recombination is stimulated, when the replication fork stalls at DNA breaks or unrepaired lesions. The tumor suppressor p53 downregulates homologous recombination independently of its transcriptional transactivation function and has been linked to enzymes of DNA recombination and replication. To study recombination with respect to replication, we utilized a SV40 virus based assay, to follow the synchronous events after primate cell infection. gamma-ray treatment at different times after viral entry unveiled an increase of interchromosomal exchange frequencies, when the damage was introduced during DNA synthesis. Elevated recombination frequencies were fully suppressed by p53. With respect to the downregulation of spontaneous recombination, we noticed a requirement for active p53 molecules, when replication started. After a transient treatment with replication inhibitors, we observed inhibition of the drug induced recombination by p53, particularly for the elongation inhibitor aphidicolin. Consequently, we propose that p53 is a surveillance factor of homologous recombination at replication forks, when they stall as a consequence of endogenous or of exogenously introduced damage.
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Registered trials
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.