ArticleDNA repair2019
RAD51D splice variants and cancer-associated mutations reveal XRCC2 interaction to be critical for homologous recombination.
Article in DNA repair, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Management of individuals with heterozygous germline pathogenic variants in RAD51C, RAD51D, and BRIP1: A clinical practice resource of the American College of Medical Genetics and Genomics (ACMG).Genetics in medicine : official journal of the American College of Medical Genetics · 2025Guideline
- Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients.Molecular medicine (Cambridge, Mass.) · 2021Pooled it
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Review
- Article
- High-throughput mapping of 6,888bioRxiv : the preprint server for biology · 2026Article
- Review
- Comprehensive RAD51C ovarian cancer variant analysis uncouples homologous recombination and replicative functions.Nature communications · 2025Article
- PRMT5-regulated splicing of DNA repair genes drives chemoresistance in breast cancer stem cells.Oncogene · 2025Article
- The human Shu complex promotes RAD51 activity by modulating RPA dynamics on ssDNA.Nature communications · 2024Article
- Characterization of alternative splicing events and prognostic signatures in gastric cancer.Cancer cell international · 2024Article
- 3Dmapper: a command line tool for BioBank-scale mapping of variants to protein structures.Bioinformatics (Oxford, England) · 2024Article
- RAD51 paralogs synergize with RAD51 to protect reversed forks from cellular nucleases.Nucleic acids research · 2023Article
- Whole Exome Sequencing reveals clinically important pathogenic mutations in DNA repair genes across lung cancer patients.American journal of cancer research · 2023Article
- Homologous recombination-deficient mutation cluster in tumor suppressorProceedings of the National Academy of Sciences of the United States of America · 2022Article
- CRISPR/Cas9‑induced saturated mutagenesis identifiesMolecular medicine reports · 2022Article
- Cytoprotective Activity of Polyamines Is Associated with the Alternative Splicing ofInternational journal of molecular sciences · 2022Article
- RAD51 paralog function in replicative DNA damage and tolerance.Current opinion in genetics & development · 2021Review
- Article
- Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
The proficiency of cancer cells to repair DNA double-strand breaks (DSBs) by homologous recombination (HR) is a key determinant in predicting response to targeted therapies such as PARP inhibitors. The RAD51 paralogs work as multimeric complexes and act downstream of BRCA1 to facilitate HR. Numerous epidemiological studies have linked RAD51 paralog mutations with hereditary cancer predisposition. Despite their substantial links to cancer, RAD51 paralog HR function has remained elusive. Here we identify isoform 1 as the functional isoform of RAD51D, whereas isoform 4 which has a large N-terminal deletion (including the Walker A motif), and isoform 6 which includes an alternate exon in the N-terminus, are non-functional. To determine the importance of this N-terminal region, we investigated the impact of cancer-associated mutations and SNPs in this variable RAD51D N-terminal region using yeast-2-hybrid and yeast-3-hybrid assays to screen for altered protein-protein interactions. We identified two cancer-associated mutations close to or within the Walker A motif (G96C and G107 V, respectively) that independently disrupt RAD51D interaction with XRCC2. We validated our yeast interaction data in human U2OS cells by co-immunoprecipitation and determined the impact of these mutations on HR-proficiency using a sister chromatid recombination reporter assay in a RAD51D knock-out cell line. Our investigation reveals that the interaction of RAD51D with XRCC2 is required for DSB repair. By characterizing the impact of cancer-associated mutations on RAD51D interactions, we aim to develop predictive models for therapeutic sensitivity and resistance in patients who harbor similar mutations in RAD51D.
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