ArticleNucleic acids research2016
Distinct binding of BRCA2 BRC repeats to RAD51 generates differential DNA damage sensitivity.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- RAD51C breast cancer-identified variants with attenuated homologous recombination function exhibit sensitivity to combined PARP1 and ATR inhibition.NAR cancer · 2026Article
- Differential roles of BRCA1 and BRCA2 in the DNA damage response revealed by isogenic V79 mutant cell lines.Mutagenesis · 2026Article
- Recent Advances in Genetic Testing and Clinical Management of Hereditary Breast and Ovarian Cancer (HBOC) in India.Cancer medicine · 2026Review
- Decoding thebioRxiv : the preprint server for biology · 2026Article
- Exploring the hereditary genetic mutational landscape of breast and ovarian cancer in Estonia.Scientific reports · 2026Article
- A single BRCA2 BRC repeat supports viability while multiple repeats ensure resilience under stress.bioRxiv : the preprint server for biology · 2026Article
- Overcoming Resistance to PARP Inhibitors in BRCA-Mutated Cancers: Mechanisms and Therapeutic Strategies.Journal of Cancer · 2026Review
- Phase 1 studies of the indenoisoquinolines LMP776 and LMP744 in patients with solid tumors and lymphomas.Cancer chemotherapy and pharmacology · 2025Article
- Distinct roles of the two BRCA2 DNA-binding domains in DNA damage repair and replication fork preservation.Cell reports · 2025Article
- Understanding genetic variations associated with familial breast cancer.World journal of surgical oncology · 2024Review
- Visualization of direct and diffusion-assisted RAD51 nucleation by full-length human BRCA2 protein.Molecular cell · 2023Article
- BRCA2 chaperones RAD51 to single molecules of RPA-coated ssDNA.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- DNA binding and RAD51 engagement by the BRCA2 C-terminus orchestrate DNA repair and replication fork preservation.Nature communications · 2023Article
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- DNA fiber combing protocol using in-house reagents and coverslips to analyze replication fork dynamics in mammalian cells.STAR protocols · 2022Article
- Single-molecule fluorescence imaging techniques reveal molecular mechanisms underlying deoxyribonucleic acid damage repair.Frontiers in bioengineering and biotechnology · 2022Review
- The Pathogenic R3052W BRCA2 Variant Disrupts Homology-Directed Repair by Failing to Localize to the Nucleus.Frontiers in genetics · 2022Article
- Improved RAD51 binders through motif shuffling based on the modularity of BRC repeats.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Hereditary breast and ovarian cancer (HBOC): review of its molecular characteristics, screening, treatment, and prognosis.Breast cancer (Tokyo, Japan) · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA2 is a multi-faceted protein critical for the proper regulation of homology-directed repair of DNA double-strand breaks. Elucidating the mechanistic features of BRCA2 is crucial for understanding homologous recombination and how patient-derived mutations impact future cancer risk. Eight centrally located BRC repeats in BRCA2 mediate binding and regulation of RAD51 on resected DNA substrates. Herein, we dissect the biochemical and cellular features of the BRC repeats tethered to the DNA binding domain of BRCA2. To understand how the BRC repeats and isolated domains of BRCA2 contribute to RAD51 binding, we analyzed both the biochemical and cellular properties of these proteins. In contrast to the individual BRC repeat units, we find that the BRC5-8 region potentiates RAD51-mediated DNA strand pairing and provides complementation functions exceeding those of BRC repeats 1-4. Furthermore, BRC5-8 can efficiently repair nuclease-induced DNA double-strand breaks and accelerate the assembly of RAD51 repair complexes upon DNA damage. These findings highlight the importance of the BRC5-8 domain in stabilizing the RAD51 filament and promoting homology-directed repair under conditions of cellular DNA damage.
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