ArticleProceedings of the National Academy of Sciences of the United States of America2010
Mapping the physical and functional interactions between the tumor suppressors p53 and BRCA2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. 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
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
25 citing papers in PubMed, 57 citations in OpenAlex.
- DNA-contact mutant p53 displaces BRCA2 from chromatin and drives R-loop-associated genome instability.Genome biology · 2026Article
- The disordered p53 transactivation domain is the target of FOXO4 and the senolytic compound FOXO4-DRI.Nature communications · 2025Article
- Distinct roles of the two BRCA2 DNA-binding domains in DNA damage repair and replication fork preservation.Cell reports · 2025Article
- DSS1 restrains BRCA2's engagement with dsDNA for homologous recombination, replication fork protection, and R-loop homeostasis.Nature communications · 2024Article
- Peptide and protein chemistry approaches to study the tumor suppressor protein p53.Organic & biomolecular chemistry · 2022Review
- DNA damage response proteins in canine cancer as potential research targets in comparative oncology.Veterinary and comparative oncology · 2022Review
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- K3326X and Other C-Terminal BRCA2 Variants Implicated in Hereditary Cancer Syndromes: A Review.Cancers · 2021Review
- Bayesian Structure Learning in Multi-layered Genomic Networks.Journal of the American Statistical Association · 2021Article
- Essential amino acid supplementation alters the p53 transcriptional response and cytokine gene expression following total knee arthroplasty.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- How do mutations affecting the breast cancer genes BRCA1 and BRCA2 cause cancer susceptibility?DNA repair · 2019Review
- Nbn-Mre11 interaction is required for tumor suppression and genomic integrity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Regulation of Apoptosis During Porcine Circovirus Type 2 Infection.Frontiers in microbiology · 2018Review
- Adaptive patterns in the p53 protein sequence of the hypoxia- and cancer-tolerant blind mole rat Spalax.BMC evolutionary biology · 2016Article
- Nuclear Localization Signal and p53 Binding Site in MAP/ERK Kinase Kinase 1 (MEKK1).Journal of cellular biochemistry · 2015Article
- Functional classification of BRCA2 DNA variants by splicing assays in a large minigene with 9 exons.Human mutation · 2015Article
- Molding BRCA2 function through its interacting partners.Cell cycle (Georgetown, Tex.) · 2015Review
- Pathological unfoldomics of uncontrolled chaos: intrinsically disordered proteins and human diseases.Chemical reviews · 2014Review
- A conserved mechanism for binding of p53 DNA-binding domain and anti-apoptotic Bcl-2 family proteins.Molecules and cells · 2014Article
- Dual-site interactions of p53 protein transactivation domain with anti-apoptotic Bcl-2 family proteins reveal a highly convergent mechanism of divergent p53 pathways.The Journal of biological chemistry · 2013Article
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
p53 maintains genome integrity either by regulating the transcription of genes involved in cell cycle, apoptosis, and DNA repair or by interacting with partner proteins. Here we provide evidence for a direct physical interaction between the tumor suppressors p53 and BRCA2. We found that the transactivation domain of p53 made specific interactions with the C-terminal oligonucleotide/oligosaccharide-binding-fold domains of BRCA2 (BRCA2(CTD)). A second distinct site situated on the p53 DNA-binding domain, bound to a region containing BRC repeats of BRCA2 (BRCA2([BRC1-8])) and may contribute synergistically for high affinity association of intact full-length proteins. Overexpression of BRCA2 and BRCA2(CTD) suppressed the transcriptional activity of p53 with a concomitant reduction in the expression of p53-target genes such as Bax and p21. Consequently, p53-mediated apoptosis was significantly attenuated by BRCA2. The observed physical association of p53 and BRCA2 may have important functional implications in the p53 transactivation-independent suppression of homologous recombination and suggests a possible interregulatory role for both proteins in apoptosis and DNA repair.
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.