ArticleProceedings of the National Academy of Sciences of the United States of America2013
Double-strand break repair by homologous recombination in primary mouse somatic cells requires BRCA1 but not the ATM kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed.
- A phase II study of talazoparib monotherapy in patients with wild-type BRCA1 and BRCA2 with a mutation in other homologous recombination genes.Nature cancer · 2022Trial
- Prognostic impact of ATM mutations in patients with metastatic colorectal cancer.Scientific reports · 2019Trial
- Base editing for precision therapeutics.Cell genomics · 2026Review
- DNA-contact mutant p53 displaces BRCA2 from chromatin and drives R-loop-associated genome instability.Genome biology · 2026Article
- Long-Term Survival Following Chemoradiation in Locoregional Recurrent GermlineAdvances in radiation oncology · 2025Article
- Integrative Analysis of DNA Methylation and microRNA Reveals GNPDA1 and SLC25A16 Related to Biopsychosocial Factors Among Taiwanese Women with a Family History of Breast Cancer.Journal of personalized medicine · 2025Article
- Construction of a TAT-Cas9-EGFP Site-Specific Integration Eukaryotic Cell Line Using Efficient PEG10 Modification.International journal of molecular sciences · 2025Article
- Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024Review
- BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair.Molecular cell · 2024Article
- Enhanced efficacy of combined fluzoparib and chidamide targeting in natural killer/T-cell lymphoma.Annals of hematology · 2023Article
- Inactive PARP1 causes embryonic lethality and genome instability in a dominant-negative manner.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- IDDoR: a novel reporter mouse system for simultaneous and quantitative in vivo analysis of both DNA double-strand break repair pathways.Protein & cell · 2023Article
- MDM2 antagonists promote CRISPR/Cas9-mediated precise genome editing in sheep primary cells.Molecular therapy. Nucleic acids · 2023Article
- Transgenic mice harboring direct repeat substrates reveal key underlying causes of homologous recombination in vivo.DNA repair · 2022Review
- Review
- To indel or not to indel: Factors influencing mutagenesis during chromosomal break end joining.DNA repair · 2022Review
- Characterisation of protein-truncating and missense variants inJournal of medical genetics · 2022Article
- Development of transgenic Daphnia magna for visualizing homology-directed repair of DNA.Scientific reports · 2022Article
- A Lack of Effectiveness in the ATM-Orchestrated DNA Damage Response Contributes to the DNA Repair Defect of HPV-Positive Head and Neck Cancer Cells.Frontiers in oncology · 2022Article
- A non-canonical, interferon-independent signaling activity of cGAMP triggers DNA damage response signaling.Nature communications · 2021Article
9 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
Homology-directed repair (HDR) is a critical pathway for the repair of DNA double-strand breaks (DSBs) in mammalian cells. Efficient HDR is thought to be crucial for maintenance of genomic integrity during organismal development and tumor suppression. However, most mammalian HDR studies have focused on transformed and immortalized cell lines. We report here the generation of a Direct Repeat (DR)-GFP reporter-based mouse model to study HDR in primary cell types derived from diverse lineages. Embryonic and adult fibroblasts from these mice as well as cells derived from mammary epithelium, ovary, and neonatal brain were observed to undergo HDR at I-SceI endonuclease-induced DSBs at similar frequencies. When the DR-GFP reporter was crossed into mice carrying a hypomorphic mutation in the breast cancer susceptibility gene Brca1, a significant reduction in HDR was detected, showing that BRCA1 is critical for HDR in somatic cell types. Consistent with an HDR defect, Brca1 mutant mice are highly sensitive to the cross-linking agent mitomycin C. By contrast, loss of the DSB signaling ataxia telangiectasia-mutated (ATM) kinase did not significantly alter HDR levels, indicating that ATM is dispensable for HDR. Notably, chemical inhibition of ATM interfered with HDR. The DR-GFP mouse provides a powerful tool for dissecting the genetic requirements of HDR in a diverse array of somatic cell types in a normal, nontransformed cellular milieu.
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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.