ArticlePLoS computational biology2015
Integrated Stochastic Model of DNA Damage Repair by Non-homologous End Joining and p53/p21-Mediated Early Senescence Signalling.
Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
- Removal of aging microenvironment of bone defects can effectively promote bone defect repair.Journal of translational medicine · 2026Article
- AI-based methods for the assessment of DNA damage and repair mechanisms.Frontiers in systems biology · 2026Review
- TOPAS-Tissue: A Framework for the Simulation of the Biological Response to Ionizing Radiation at the Multi-Cellular Level.International journal of molecular sciences · 2024Article
- Nimbolide Exhibits Potent Anticancer Activity Through ROS-Mediated ER Stress and DNA Damage in Human Non-small Cell Lung Cancer Cells.Applied biochemistry and biotechnology · 2024Article
- Effects of Differing Underlying Assumptions in In Silico Models on Predictions of DNA Damage and Repair.Radiation research · 2023Article
- Review
- Review
- Modeling of DNA Damage Repair and Cell Response in Relation to p53 System Exposed to Ionizing Radiation.International journal of molecular sciences · 2022Article
- Cellular Senescence: Molecular Targets, Biomarkers, and Senolytic Drugs.International journal of molecular sciences · 2022Review
- Article
- Capturing Biomarkers and Molecular Targets in Cellular Landscapes From Dynamic Reaction Network Models and Machine Learning.Frontiers in oncology · 2021Review
- p16Frontiers in immunology · 2021Article
- Role of p53 in the Regulation of Cellular Senescence.Biomolecules · 2020Review
- Boolean model of growth signaling, cell cycle and apoptosis predicts the molecular mechanism of aberrant cell cycle progression driven by hyperactive PI3K.PLoS computational biology · 2019Article
- Mechanistic Modelling of Radiation Responses.Cancers · 2019Review
- Chlorogenic acid effectively treats cancers through induction of cancer cell differentiation.Theranostics · 2019Article
- Senescence Inducer Shikonin ROS-Dependently Suppressed Lung Cancer Progression.Frontiers in pharmacology · 2018Article
- Systems modelling ageing: from single senescent cells to simple multi-cellular models.Essays in biochemistry · 2017Review
- Modelling the molecular mechanisms of aging.Bioscience reports · 2017Review
- A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.BMC systems biology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Unrepaired or inaccurately repaired DNA damage can lead to a range of cell fates, such as apoptosis, cellular senescence or cancer, depending on the efficiency and accuracy of DNA damage repair and on the downstream DNA damage signalling. DNA damage repair and signalling have been studied and modelled in detail separately, but it is not yet clear how they integrate with one another to control cell fate. In this study, we have created an integrated stochastic model of DNA damage repair by non-homologous end joining and of gamma irradiation-induced cellular senescence in human cells that are not apoptosis-prone. The integrated model successfully explains the changes that occur in the dynamics of DNA damage repair after irradiation. Simulations of p53/p21 dynamics after irradiation agree well with previously published experimental studies, further validating the model. Additionally, the model predicts, and we offer some experimental support, that low-dose fractionated irradiation of cells leads to temporal patterns in p53/p21 that lead to significant cellular senescence. The integrated model is valuable for studying the processes of DNA damage induced cell fate and predicting the effectiveness of DNA damage related medical interventions at the cellular level.
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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.