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    Mechanistic modelling of slow and fast NHEJ DNA repair pathways following radiation for G0/G1 normal tissue cells

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    Authors
    Qi, Yaping
    Warmenhoven, John
    Henthorn, Nicholas
    Ingram, Samuel
    Xu, X. G.
    Kirkby, Karen J
    Merchant, Michael J
    Affiliation
    School of Nuclear Science and Technology, University of Science and Technology of China, Hefei 230026, China.
    Issue Date
    2021
    
    Metadata
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    Abstract
    Mechanistic in silico models can provide insight into biological mechanisms and highlight uncertainties for experimental investigation. Radiation-induced double-strand breaks (DSBs) are known to be toxic lesions if not repaired correctly. Non-homologous end joining (NHEJ) is the major DSB-repair pathway available throughout the cell cycle and, recently, has been hypothesised to consist of a fast and slow component in G0/G1. The slow component has been shown to be resection-dependent, requiring the nuclease Artemis to function. However, the pathway is not yet fully understood. This study compares two hypothesised models, simulating the action of individual repair proteins on DSB ends in a step-by-step manner, enabling the modelling of both wild-type and protein-deficient cell systems. Performance is benchmarked against experimental data from 21 cell lines and 18 radiation qualities. A model where resection-dependent and independent pathways are entirely separated can only reproduce experimental repair kinetics with additional restraints on end motion and protein recruitment. However, a model where the pathways are entwined was found to effectively fit without needing additional mechanisms. It has been shown that DaMaRiS is a useful tool when analysing the connections between resection-dependent and independent NHEJ repair pathways and robustly matches with experimental results from several sources.
    Citation
    Qi Y, Warmenhoven JW, Henthorn NT, Ingram SP, Xu XG, Kirkby KJ, et al. Mechanistic Modelling of Slow and Fast NHEJ DNA Repair Pathways Following Radiation for G0/G1 Normal Tissue Cells. Cancers. 2021 May 3;13(9):2202.
    Journal
    Cancers
    URI
    http://hdl.handle.net/10541/624066
    DOI
    10.3390/cancers13092202
    PubMed ID
    34063683
    Additional Links
    https://dx.doi.org/10.3390/cancers13092202
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.3390/cancers13092202
    Scopus Count
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