ArticleThe Journal of biological chemistry2014
Homologous recombination is a primary pathway to repair DNA double-strand breaks generated during DNA rereplication.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Transcriptomic analysis of laser-capture microdissected tumors reveals RAD51AP1 as a tumor-specific marker associated progression from pancreatic intraepithelial neoplasia to invasive pancreatic cancer.Cancer cell international · 2025Article
- RAD51 restricts DNA over-replication from re-activated origins.The EMBO journal · 2024Article
- Dual blockade of BRD4 and ATR/WEE1 pathways exploitsResearch square · 2023Article
- Review
- Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress.International journal of molecular sciences · 2022Review
- DNA nicks induce mutational signatures associated with BRCA1 deficiency.Nature communications · 2022Article
- Inhibition of miR-1193 leads to synthetic lethality in glioblastoma multiforme cells deficient of DNA-PKcs.Cell death & disease · 2020Article
- PAICS contributes to gastric carcinogenesis and participates in DNA damage response by interacting with histone deacetylase 1/2.Cell death & disease · 2020Article
- A Lamin-Binding Ligand Inhibits Homologous Recombination Repair of DNA Double-Strand Breaks.ACS central science · 2018Article
- Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cells.Communications biology · 2018Article
- Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Replication fork instability and the consequences of fork collisions from rereplication.Genes & development · 2016Review
- Chromosomal Replication Complexity: A Novel DNA Metrics and Genome Instability Factor.PLoS genetics · 2016Review
- Polq-Mediated End Joining Is Essential for Surviving DNA Double-Strand Breaks during Early Zebrafish Development.Cell reports · 2016Article
- Static and Dynamic Factors Limit Chromosomal Replication Complexity in Escherichia coli, Avoiding Dangers of Runaway Overreplication.Genetics · 2016Article
- DNA polymerases δ and λ cooperate in repairing double-strand breaks by microhomology-mediated end-joining in Saccharomyces cerevisiae.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability.Nucleic acids research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Re-initiation of DNA replication at origins within a given cell cycle would result in DNA rereplication, which can lead to genome instability and tumorigenesis. DNA rereplication can be induced by loss of licensing control at cellular replication origins, or by viral protein-driven multiple rounds of replication initiation at viral origins. DNA double-strand breaks (DSBs) are generated during rereplication, but the mechanisms of how these DSBs are repaired to maintain genome stability and cell viability are poorly understood in mammalian cells. We generated novel EGFP-based DSB repair substrates, which specifically monitor the repair of rereplication-associated DSBs. We demonstrated that homologous recombination (HR) is an important mechanism to repair rereplication-associated DSBs, and sister chromatids are used as templates for such HR-mediated DSB repair. Micro-homology-mediated non-homologous end joining (MMEJ) can also be used but to a lesser extent compared to HR, whereas Ku-dependent classical non-homologous end joining (C-NHEJ) has a minimal role to repair rereplication-associated DSBs. In addition, loss of HR activity leads to severe cell death when rereplication is induced. Therefore, our studies identify HR, the most conservative repair pathway, as the primary mechanism to repair DSBs upon rereplication.
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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.