ArticleNucleic acids research2012
A dual role of BRCA1 in two distinct homologous recombination mediated repair in response to replication arrest.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Differential roles of BRCA1 and BRCA2 in the DNA damage response revealed by isogenic V79 mutant cell lines.Mutagenesis · 2026Article
- VPA mediates bidirectional regulation of cell cycle progression through the PPP2R2A-Chk1 signaling axis in response to HU.Cell death & disease · 2023Article
- Regulation of BRCA1 stability through the tandem UBX domains of isoleucyl-tRNA synthetase 1.Nature communications · 2022Article
- A Novel Role for RNF126 in the Promotion of G2 Arrest via Interaction With 14-3-3σ.International journal of radiation oncology, biology, physics · 2022Article
- TheGenes & development · 2021Article
- Inhibition of c-MET increases the antitumour activity of PARP inhibitors in gastric cancer models.Journal of cellular and molecular medicine · 2020Article
- Fragile site instability: measuring more than breaks.Oncoscience · 2020Article
- ATR/CHK1 inhibitors and cancer therapy.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2018Review
- DNA repair and cell cycle checkpoint defects in a mouse model of 'BRCAness' are partially rescued by 53BP1 deletion.Cell cycle (Georgetown, Tex.) · 2018Article
- The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats.International journal of molecular sciences · 2017Article
- Loss of BRCA1 or BRCA2 markedly increases the rate of base substitution mutagenesis and has distinct effects on genomic deletions.Oncogene · 2017Article
- FANCJ at the FORK.Mutation research · 2016Review
- Stalled replication forks within heterochromatin require ATRX for protection.Cell death & disease · 2016Article
- RNF126 promotes homologous recombination via regulation of E2F1-mediated BRCA1 expression.Oncogene · 2016Article
- EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair.PLoS genetics · 2015Article
- BRCA1 Mutation: A Predictive Marker for Radiation Therapy?International journal of radiation oncology, biology, physics · 2015Review
- p53 suppresses hyper-recombination by modulating BRCA1 function.DNA repair · 2015Article
- The TMPRSS2-ERG Gene Fusion Blocks XRCC4-Mediated Nonhomologous End-Joining Repair and Radiosensitizes Prostate Cancer Cells to PARP Inhibition.Molecular cancer therapeutics · 2015Article
- 53BP1 promotes microhomology-mediated end-joining in G1-phase cells.Nucleic acids research · 2015Article
- Oxidative stress diverts tRNA synthetase to nucleus for protection against DNA damage.Molecular cell · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Homologous recombination (HR) is a major mechanism utilized to repair blockage of DNA replication forks. Here, we report that a sister chromatid exchange (SCE) generated by crossover-associated HR efficiently occurs in response to replication fork stalling before any measurable DNA double-strand breaks (DSBs). Interestingly, SCE produced by replication fork collapse following DNA DSBs creation is specifically suppressed by ATR, a central regulator of the replication checkpoint. BRCA1 depletion leads to decreased RPA2 phosphorylation (RPA2-P) following replication fork stalling but has no obvious effect on RPA2-P following replication fork collapse. Importantly, we found that BRCA1 promotes RAD51 recruitment and SCE induced by replication fork stalling independent of ATR. In contrast, BRCA1 depletion leads to a more profound defect in RAD51 recruitment and SCE induced by replication fork collapse when ATR is depleted. We concluded that BRCA1 plays a dual role in two distinct HR-mediated repair upon replication fork stalling and collapse. Our data established a molecular basis for the observation that defective BRCA1 leads to a high sensitivity to agents that cause replication blocks without being associated with DSBs, and also implicate a novel mechanism by which loss of cell cycle checkpoints promotes BRCA1-associated tumorigenesis via enhancing HR defect resulting from BRCA1 deficiency.
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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.