ArticleOncogene2004
The interaction of p53 with replication protein A mediates suppression of homologous recombination.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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.
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
55 citing papers in PubMed, 103 citations in OpenAlex.
- Proteomic Analysis of TCGA Data Reveals Limited Prognostic Value of p53 but Suggests BAX as a Potential Survival Marker in Cervical Carcinoma.International journal of molecular sciences · 2026Article
- RPA-ssDNA co-phase separation facilitates RAD51 enrichment during homologous recombination.Nucleic acids research · 2026Article
- Interdependent roles of BRCA1, CtBP, estrogen, and NADH/NAD+ ratio in error-prone repair, breast cancer initiation, and metastasis.Molecular biology reports · 2026Review
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Improving homology-directed repair by small molecule agents for genetic engineering in unconventional yeast?-Learning from the engineering of mammalian systems.Microbial biotechnology · 2024Review
- Review
- Article
- Alterations in the p53 isoform ratio govern breast cancer cell fate in response to DNA damage.Cell death & disease · 2022Article
- A Critical Role for p53 during the HPV16 Life Cycle.Microbiology spectrum · 2022Article
- PPIP5K2 promotes colorectal carcinoma pathogenesis through facilitating DNA homologous recombination repair.Oncogene · 2021Article
- p53 isoforms differentially impact on the POLι dependent DNA damage tolerance pathway.Cell death & disease · 2021Article
- On the specificity of protein-protein interactions in the context of disorder.The Biochemical journal · 2021Review
- Article
- Multiple biochemical properties of the p53 molecule contribute to activation of polymerase iota-dependent DNA damage tolerance.Nucleic acids research · 2020Article
- Dual inhibition of DNA-PK and DNA polymerase theta overcomes radiation resistance induced by p53 deficiency.NAR cancer · 2020Article
- The Δ133p53 Isoforms, Tuners of the p53 Pathway.Cancers · 2020Review
- Dynamic elements of replication protein A at the crossroads of DNA replication, recombination, and repair.Critical reviews in biochemistry and molecular biology · 2020Review
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- p53 and its isoforms in DNA double-stranded break repair.Journal of Zhejiang University. Science. B · 2019Review
- Drugging in the absence of p53.Journal of molecular cell biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor protein p53 is emerging as a central regulator of homologous recombination (HR) processes and DNA replication. P53 may downregulate HR through multiple mechanisms including the reported associations with the Rad51 and Rad54 recombinases, and the BLM and WRN helicases. Here, we investigated whether the interaction of p53 with human replication protein A (RPA) is necessary for the regulation of HR. By employing a plasmid-based HR assay in p53-null H1299 lung carcinoma cells, we studied the HR-suppressing properties of a panel of p53 mutants, which varied in their ability to interact with RPA. Both wild-type p53 and a transactivation-deficient p53 mutant (L22Q/W23S) suppressed HR and prevented RPA binding to ssDNA in vitro and in vivo. Conversely, p53 mutations that specifically disrupt the RPA-binding domain, while not compromising p53 transactivation function (D48H/D49H and W53S/F54S), did not affect HR. Suppression of HR was also not seen with missense mutations in the p53 core domain (His175 and His273), which retained the ability to interact with RPA, suggesting that the disruption of additional binding interactions of p53, for example, with Rad51 or recombination intermediates, also impacts on HR. We hypothesize that sequestration of RPA by p53 at the sites of recombination is one means by which p53 can inhibit HR processes. Our data support and extend the previously formulated 'dual model' of p53's role as guardian of the genome.
Indexed as
Identifiers
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.