ArticleCell cycle (Georgetown, Tex.)2015
High levels of RAD51 perturb DNA replication elongation and cause unscheduled origin firing due to impaired CHK1 activation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- AZD6738 overcomes acquired olaparib resistance in BRCA1 mutation triple-negative breast cancer through down-regulation of BRCA2 and RAD51.Scientific reports · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Synthesis and new DNA targeting activity of 6- and 7-tert-butylfascaplysins.Scientific reports · 2024Article
- The Inability to Disassemble Rad51 Nucleoprotein Filaments Leads to Aberrant Mitosis and Cell Death.Biomedicines · 2023Article
- The location and development of Replicon Cluster Domains in early replicating DNA.Wellcome open research · 2023Article
- Studying the DNA damage response pathway in hematopoietic canine cancer cell lines, a necessary step for finding targets to generate new therapies to treat cancer in dogs.Frontiers in veterinary science · 2023Article
- Partial Reduction inInternational journal of molecular sciences · 2022Article
- ATR Contributes More Than ATM in Intra-S-Phase Checkpoint Activation after IR, and DNA-PKcs Facilitates Recovery: Evidence for Modular Integration of ATM/ATR/DNA-PKcs Functions.International journal of molecular sciences · 2022Article
- Efficient DNA Repair Mitigates Replication Stress Resulting in Less Immunogenic Cytosolic DNA in Radioresistant Breast Cancer Stem Cells.Frontiers in immunology · 2022Article
- Mechanisms of damage tolerance and repair during DNA replication.Nucleic acids research · 2021Review
- DNA Damage Response during Replication Correlates with CIN70 Score and Determines Survival in HNSCC Patients.Cancers · 2021Article
- Targeting the DNA replication stress phenotype of KRAS mutant cancer cells.Scientific reports · 2021Article
- GIP1 and GIP2 Contribute to the Maintenance of Genome Stability at the Nuclear Periphery.Frontiers in plant science · 2021Article
- Article
- Article
- RAD51 and mitotic function of mus81 are essential for recovery from low-dose of camptothecin in the absence of the WRN exonuclease.Nucleic acids research · 2019Article
- Tools To Live By: Bacterial DNA Structures Illuminate Cancer.Trends in genetics : TIG · 2019Review
- The Post-Synaptic Function of Brca2.Scientific reports · 2019Article
- Rescue of collapsed replication forks is dependent on NSMCE2 to prevent mitotic DNA damage.PLoS genetics · 2019Article
- The F-Box Domain-Dependent Activity of EMI1 Regulates PARPi Sensitivity in Triple-Negative Breast Cancers.Molecular cell · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to replication stress ATR signaling through CHK1 controls the intra-S checkpoint and is required for the maintenance of genomic integrity. Homologous recombination (HR) comprises a series of interrelated pathways that function in the repair of DNA double strand breaks and interstrand crosslinks. In addition, HR, with its key player RAD51, provides critical support for the recovery of stalled forks during replication. High levels of RAD51 are regularly found in various cancers, yet little is known about the effect of the increased RAD51 expression on intra-S checkpoint signaling. Here, we describe a role for RAD51 in driving genomic instability caused by impaired replication and intra-S mediated CHK1 signaling by studying an inducible RAD51 overexpression model as well as 10 breast cancer cell lines. We demonstrate that an excess of RAD51 decreases I-Sce-I mediated HR despite formation of more RAD51 foci. Cells with high RAD51 levels display reduced elongation rates and excessive dormant origin firing during undisturbed growth and after damage, likely caused by impaired CHK1 activation. In consequence, the inability of cells with a surplus of RAD51 to properly repair complex DNA damage and to resolve replication stress leads to higher genomic instability and thus drives tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.