ArticleOncogene2000
Dissociation of p53-mediated suppression of homologous recombination from G1/S cell cycle checkpoint control.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 101 citations in OpenAlex.
- Effects of p53 and ATRX inhibition on telomeric recombination in aging fibroblasts.Frontiers in oncology · 2024Article
- Inhibition of p53 and ATRX increases telomeric recombination in primary fibroblasts.FEBS open bio · 2023Article
- Many Functions of Telomerase Components: Certainties, Doubts, and Inconsistencies.International journal of molecular sciences · 2022Review
- Alterations in the p53 isoform ratio govern breast cancer cell fate in response to DNA damage.Cell death & disease · 2022Article
- Utility of Homologous Recombination Deficiency Biomarkers Across Cancer Types.JCO precision oncology · 2022Article
- Utility of Homologous Recombination Deficiency Biomarkers Across Cancer Types.JCO precision oncology · 2021Article
- Evaluation of the Response of HOS and Saos-2 Osteosarcoma Cell Lines When Exposed to Different Sizes and Concentrations of Silver Nanoparticles.BioMed research international · 2021Article
- p53 and its isoforms in DNA double-stranded break repair.Journal of Zhejiang University. Science. B · 2019Review
- A new role for a tumor-suppressing protein.eLife · 2018Article
- SOCS1 regulates senescence and ferroptosis by modulating the expression of p53 target genes.Aging · 2017Article
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- Influence of Human p53 on Plant Development.PloS one · 2016Article
- p53 suppresses hyper-recombination by modulating BRCA1 function.DNA repair · 2015Article
- p53 isoform Δ113p53/Δ133p53 promotes DNA double-strand break repair to protect cell from death and senescence in response to DNA damage.Cell research · 2015Article
- p53 modulates homologous recombination at I-SceI-induced double-strand breaks through cell-cycle regulation.Oncogene · 2013Article
- p53 null fluorescent yellow direct repeat (FYDR) mice have normal levels of homologous recombination.DNA repair · 2011Article
- Expression of RAD51, BRCA1 and P53 does not correlate with cellular radiosensitivity of normal human fibroblasts.Irish journal of medical science · 2011Article
- Article
- Exonuclease function of human Mre11 promotes deletional nonhomologous end joining.The Journal of biological chemistry · 2009Article
- Threshold effects of nitric oxide-induced toxicity and cellular responses in wild-type and p53-null human lymphoblastoid cells.Chemical research in toxicology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The tumor suppressor p53 is considered as the guardian of the genome which is activated following genotoxic stress. In many cell types, p53 mediates G1 cell cycle arrest as the predominant cellular response. Inactivation of wild-type p53 leads to loss of G1/S checkpoint control and to genomic instability, including increased spontaneous homologous recombination (HR). To determine whether regulation of the G1/S checkpoint is required for suppression of HR, we assessed recombination events using a plasmid substrate that stably integrated into the genome of p53-null mouse fibroblasts. Exogenous expression of a temperature-sensitive p53 protein (Ala135 to Val), which had lost trans-activation function and could not regulate G1/S transition when in mutant conformation, reduced HR rates to the same extent as wild-type p53. Furthermore, a p53 construct with an alternatively-spliced carboxy terminus also retained this ability in the absence of both activities, G1/S control and non-sequence specific DNA binding as mediated by the carboxy terminus. Our data dissociate regulation of HR by p53 from its role as a cell cycle checkpoint protein. The results support a model which extends p53's role as a guardian of the genome to include transactivation-independent regulatory functions in DNA repair, replication and recombination.
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What OpenQuestion holds
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.