ArticlePLoS genetics2011
Plasticity of BRCA2 function in homologous recombination: genetic interactions of the PALB2 and DNA binding domains.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 88 citations in OpenAlex.
- A single BRCA2 BRC repeat supports viability while multiple repeats ensure resilience under stress.bioRxiv : the preprint server for biology · 2026Article
- Moss BRCA2 lacking the canonical DNA-binding domain promotes homologous recombination and binds to DNA.Nucleic acids research · 2025Article
- BRCA2 C-terminal clamp restructures RAD51 dimers to bind B-DNA for replication fork stability.Molecular cell · 2025Article
- Mechanism of BCDX2-mediated RAD51 nucleation on short ssDNA stretches and fork DNA.Nucleic acids research · 2024Article
- DSS1 restrains BRCA2's engagement with dsDNA for homologous recombination, replication fork protection, and R-loop homeostasis.Nature communications · 2024Article
- Genetic analysis of PALB2 gene WD40 domain in canine mammary tumour patients.Veterinary medicine and science · 2024Article
- BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair.Molecular cell · 2024Article
- BRCA1/2 reversion mutations in a pan-cancer cohort.Cancer science · 2024Article
- Analysis of the indispensable RAD51 cofactor BRCA2 inLife science alliance · 2024Article
- Characterization of BRCA2 R3052Q variant in mice supports its functional impact as a low-risk variant.Cell death & disease · 2023Article
- Visualization of direct and diffusion-assisted RAD51 nucleation by full-length human BRCA2 protein.Molecular cell · 2023Article
- Repair of DNA double-strand breaks in plant meiosis: role of eukaryotic RecA recombinases and their modulators.Plant reproduction · 2023Review
- DNA binding and RAD51 engagement by the BRCA2 C-terminus orchestrate DNA repair and replication fork preservation.Nature communications · 2023Article
- Transgenic mice harboring direct repeat substrates reveal key underlying causes of homologous recombination in vivo.DNA repair · 2022Review
- Evidence for reduced BRCA2 functional activity in Homo sapiens after divergence from the chimpanzee-human last common ancestor.Cell reports · 2022Article
- Review
- Mechanism of mitotic recombination: insights from C. elegans.Current opinion in genetics & development · 2021Review
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- Missense Variants of Uncertain Significance: A Powerful Genetic Tool for Function Discovery with Clinical Implications.Cancers · 2021Review
- Role of BRCA2 DNA-binding and C-terminal domain in its mobility and conformation in DNA repair.eLife · 2021Article
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 3 countries.
Funding
Abstract
The breast cancer suppressor BRCA2 is essential for the maintenance of genomic integrity in mammalian cells through its role in DNA repair by homologous recombination (HR). Human BRCA2 is 3,418 amino acids and is comprised of multiple domains that interact with the RAD51 recombinase and other proteins as well as with DNA. To gain insight into the cellular function of BRCA2 in HR, we created fusions consisting of various BRCA2 domains and also introduced mutations into these domains to disrupt specific protein and DNA interactions. We find that a BRCA2 fusion peptide deleted for the DNA binding domain and active in HR is completely dependent on interaction with the PALB2 tumor suppressor for activity. Conversely, a BRCA2 fusion peptide deleted for the PALB2 binding domain is dependent on an intact DNA binding domain, providing a role for this conserved domain in vivo; mutagenesis suggests that both single-stranded and double-stranded DNA binding activities in the DNA binding domain are required for its activity. Given that PALB2 itself binds DNA, these results suggest alternative mechanisms to deliver RAD51 to DNA. In addition, the BRCA2 C terminus contains both RAD51-dependent and -independent activities which are essential to HR in some contexts. Finally, binding the small peptide DSS1 is essential for activity when its binding domain is present, but not when it is absent. Our results reveal functional redundancy within the BRCA2 protein and emphasize the plasticity of this large protein built for optimal HR function in mammalian cells. The occurrence of disease-causing mutations throughout BRCA2 suggests sub-optimal HR from a variety of domain modulations.
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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.