ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2011
Regulatory networks integrating cell cycle control with DNA damage checkpoints and double-strand break repair.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 139 citations in OpenAlex.
- Synthetic lethality and DNA damage response targeting in cancer stem cells: a comprehensive review.Discover oncology · 2026Review
- Enhanced Ciliogenesis of Human Bronchial Epithelial Cells by Simulated Microgravity.Life (Basel, Switzerland) · 2025Article
- Revisiting an old therapy for new, promising combinations: Biology and perspectives of lomustine in glioma treatment.Neuro-oncology · 2025Review
- Cohesin reconstitution and homologous recombination repair of DNA double-strand breaks in late mitosis.eLife · 2025Article
- Article
- Anlotinib suppresses the DNA damage response by disrupting SETD1A and inducing p53-dependent apoptosis in Transformed Follicular Lymphoma.International journal of medical sciences · 2024Article
- Integrating Radioprotective Agents into Post-Mastectomy Radiotherapy: Optimization of Reconstructive Outcomes in Breast Cancer.Journal of surgery and research · 2024Article
- Bladder Cancer Treatments in the Age of Personalized Medicine: A Comprehensive Review of Potential Radiosensitivity Biomarkers.Biomarker insights · 2024Review
- The DNA Damage Repair Function of Fission Yeast CK1 Involves Targeting Arp8, a Subunit of the INO80 Chromatin Remodeling Complex.Molecular and cellular biology · 2024Article
- Immune modulation and prognostic significance of MCM10 in pan-cancer: a comprehensive analysis.American journal of translational research · 2023Article
- Ganetespib selectively sensitizes cancer cells for proximal and distal spread-out Bragg peak proton irradiation.Radiation oncology (London, England) · 2022Article
- Resistance to CDK4/6 Inhibitors in Estrogen Receptor-Positive Breast Cancer.International journal of molecular sciences · 2021Review
- Biodosimetry in interventional radiology: cutaneous-based immunoassay for anticipating risks of dermatitis.European radiology · 2021Article
- Schizosaccharomyces pombe KAT5 contributes to resection and repair of a DNA double-strand break.Genetics · 2021Article
- Sustained CHK2 activity, but not ATM activity, is critical to maintain a G1 arrest after DNA damage in untransformed cells.BMC biology · 2021Article
- Nickel carcinogenesis mechanism: cell cycle dysregulation.Environmental science and pollution research international · 2021Review
- Article
- Mitotic entry upon Topo II catalytic inhibition is controlled by Chk1 and Plk1.The FEBS journal · 2020Article
- FANCJ compensates for RAP80 deficiency and suppresses genomic instability induced by interstrand cross-links.Nucleic acids research · 2020Article
- Targeting the DNA Damage Response to Overcome Cancer Drug Resistance in Glioblastoma.International journal of molecular sciences · 2020Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Double-strand breaks (DSBs), arising from exposure to exogenous clastogens or as a by-product of endogenous cellular metabolism, pose grave threats to genome integrity. DSBs can sever whole chromosomes, leading to chromosomal instability, a hallmark of cancer. Healing broken DNA takes time, and it is therefore essential to temporarily halt cell division while DSB repair is underway. The seminal discovery of cyclin-dependent kinases as master regulators of the cell cycle unleashed a series of studies aimed at defining how the DNA damage response network delays cell division. These efforts culminated with the identification of Cdc25, the protein phosphatase that activates Cdc2/Cdk1, as a critical target of the checkpoint kinase Chk1. However, regulation works both ways, as recent studies have revealed that Cdc2 activity and cell cycle position determine whether DSBs are repaired by non-homologous end-joining or homologous recombination (HR). Central to this regulation are the proteins that initiate the processing of DNA ends for HR repair, Mre11-Rad50-Nbs1 protein complex and Ctp1/Sae2/CtIP, and the checkpoint kinases Tel1/ATM and Rad3/ATR. Here, we review recent findings and provide insight on how proteins that regulate cell cycle progression affect DSB repair, and, conversely how proteins that repair DSBs affect cell cycle progression.
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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.