ArticleOncogene2004
p53 protects from replication-associated DNA double-strand breaks in mammalian cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 48 citations in OpenAlex.
- 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
- 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
- FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.Nucleic acids research · 2016Article
- Article
- Revisiting p53 for cancer-specific chemo- and radiotherapy: ten years after.Cell cycle (Georgetown, Tex.) · 2014Review
- Diminished origin-licensing capacity specifically sensitizes tumor cells to replication stress.Molecular cancer research : MCR · 2013Article
- 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
- A reduction of licensed origins reveals strain-specific replication dynamics in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- The G1 phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification.Cell division · 2011Article
- Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repair.Molecular cell · 2010Article
- p53 suppression overwhelms DNA polymerase eta deficiency in determining the cellular UV DNA damage response.DNA repair · 2007Article
- Replicational stress selects for p53 mutation.Cell cycle (Georgetown, Tex.) · 2007Article
- p53 mediates senescence-like arrest induced by chronic replicational stress.Molecular and cellular biology · 2007Article
- Increased common fragile site expression, cell proliferation defects, and apoptosis following conditional inactivation of mouse Hus1 in primary cultured cells.Molecular biology of the cell · 2007Article
- Threshold effects of nitric oxide-induced toxicity and cellular responses in wild-type and p53-null human lymphoblastoid cells.Chemical research in toxicology · 2006Article
- Transcription-independent suppression of DNA synthesis by p53 in sperm-irradiated mouse zygotes.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
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic instability caused by mutations in the p53 gene is generally thought to be due to a loss of the DNA damage response that controls checkpoint functions and apoptosis. Cells with mutant p53 exhibit high levels of homologous recombination (HR). This could be an indirect consequence of the loss of DNA damage response or p53 could have a direct role in HR. Here, we report that p53-/- mouse embryonic fibroblasts (MEFs) exhibit higher levels of the RAD51 protein and increased level of spontaneous RAD51 foci Agents that stall replication forks, for example, hydroxyurea (HU), potently induce HR repair and RAD51 foci. To test if the increase in RAD51 foci in p53-/- MEFs was due to an increased level of damage during replication, we measured the formation of DNA double-strand breaks (DSBs) in p53+/+ and p53-/- MEFs following treatments with HU. We found that HU induced DSBs only in p53-/- MEFs, indicating that p53 is involved in a pathway to protect stalled replication forks from being collapsed into a substrate for HR. Also, p53 is upregulated in response to agents that inhibit DNA replication, which supports our hypothesis. Finally, we observed that the DSBs produced in p53-/- MEFs did not result in a permanent arrest of replication and that they were repaired. Altogether, we suggest that the effect of p53 on HR and RAD51 levels and foci can be explained by the idea that p53 suppresses formation of recombinogenic lesions.
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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.