ArticlePloS one2013
Systems modelling of NHEJ reveals the importance of redox regulation of Ku70/80 in the dynamics of dna damage foci.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed, 19 citations in OpenAlex.
- Effects of Differing Underlying Assumptions in In Silico Models on Predictions of DNA Damage and Repair.Radiation research · 2023Article
- Modeling the interplay between DNA-PK, Artemis, and ATM in non-homologous end-joining repair in G1 phase of the cell cycle.Journal of biological physics · 2019Article
- Molecular Mechanisms of DNA Replication and Repair Machinery: Insights from Microscopic Simulations.Advanced theory and simulations · 2019Article
- Article
- 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
- SBMLsqueezer 2: context-sensitive creation of kinetic equations in biochemical networks.BMC systems biology · 2015Article
- Integrated Stochastic Model of DNA Damage Repair by Non-homologous End Joining and p53/p21-Mediated Early Senescence Signalling.PLoS computational biology · 2015Article
- Computational modelling of the regulation of Insulin signalling by oxidative stress.BMC systems biology · 2013Article
- P21-PARP-1 pathway is involved in cigarette smoke-induced lung DNA damage and cellular senescence.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The presence of DNA double-stranded breaks in a mammalian cell typically activates the Non-Homologous End Joining (NHEJ) pathway to repair the damage and signal to downstream systems that govern cellular decisions such as apoptosis or senescence. The signalling system also stimulates effects such as the generation of reactive oxygen species (ROS) which in turn feed back into the damage response. Although the overall process of NHEJ is well documented, we know little of the dynamics and how the system operates as a whole. We have developed a computational model which includes DNA Protein Kinase (DNA-PK) dependent NHEJ (D-NHEJ) and back-up NHEJ mechanisms (B-NHEJ) and use it to explain the dynamic response to damage induced by different levels of gamma irradiation in human fibroblasts. Our work suggests that the observed shift from fast to slow repair of DNA damage foci at higher levels of damage cannot be explained solely by inherent stochasticity in the NHEJ system. Instead, our model highlights the importance of Ku oxidation which leads to increased Ku dissociation rates from DNA damage foci and shifts repair in favour of the less efficient B-NHEJ system.
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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.