Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress

Under acute perturbations from outer environment, a normal cell can trigger cellular self-defense mechanism in response to genome stress. To investigate the kinetics of cellular self-repair process at single cell level further, a model of DNA damage generating and repair is proposed under acute Ion...

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Main Authors: Qi, Jinpeng, Ding, Yongsheng, Zhu, Ying, Wu, Yizhi
Format: Online
Language:English
Published: Public Library of Science 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153456/
id pubmed-3153456
recordtype oai_dc
spelling pubmed-31534562011-08-19 Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress Qi, Jinpeng Ding, Yongsheng Zhu, Ying Wu, Yizhi Research Article Under acute perturbations from outer environment, a normal cell can trigger cellular self-defense mechanism in response to genome stress. To investigate the kinetics of cellular self-repair process at single cell level further, a model of DNA damage generating and repair is proposed under acute Ion Radiation (IR) by using mathematical framework of kinetic theory of active particles (KTAP). Firstly, we focus on illustrating the profile of Cellular Repair System (CRS) instituted by two sub-populations, each of which is made up of the active particles with different discrete states. Then, we implement the mathematical framework of cellular self-repair mechanism, and illustrate the dynamic processes of Double Strand Breaks (DSBs) and Repair Protein (RP) generating, DSB-protein complexes (DSBCs) synthesizing, and toxins accumulating. Finally, we roughly analyze the capability of cellular self-repair mechanism, cellular activity of transferring DNA damage, and genome stability, especially the different fates of a certain cell before and after the time thresholds of IR perturbations that a cell can tolerate maximally under different IR perturbation circumstances. Public Library of Science 2011-08-09 /pmc/articles/PMC3153456/ /pubmed/21857915 http://dx.doi.org/10.1371/journal.pone.0022228 Text en Qi et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Qi, Jinpeng
Ding, Yongsheng
Zhu, Ying
Wu, Yizhi
spellingShingle Qi, Jinpeng
Ding, Yongsheng
Zhu, Ying
Wu, Yizhi
Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
author_facet Qi, Jinpeng
Ding, Yongsheng
Zhu, Ying
Wu, Yizhi
author_sort Qi, Jinpeng
title Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
title_short Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
title_full Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
title_fullStr Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
title_full_unstemmed Kinetic Theory Approach to Modeling of Cellular Repair Mechanisms under Genome Stress
title_sort kinetic theory approach to modeling of cellular repair mechanisms under genome stress
description Under acute perturbations from outer environment, a normal cell can trigger cellular self-defense mechanism in response to genome stress. To investigate the kinetics of cellular self-repair process at single cell level further, a model of DNA damage generating and repair is proposed under acute Ion Radiation (IR) by using mathematical framework of kinetic theory of active particles (KTAP). Firstly, we focus on illustrating the profile of Cellular Repair System (CRS) instituted by two sub-populations, each of which is made up of the active particles with different discrete states. Then, we implement the mathematical framework of cellular self-repair mechanism, and illustrate the dynamic processes of Double Strand Breaks (DSBs) and Repair Protein (RP) generating, DSB-protein complexes (DSBCs) synthesizing, and toxins accumulating. Finally, we roughly analyze the capability of cellular self-repair mechanism, cellular activity of transferring DNA damage, and genome stability, especially the different fates of a certain cell before and after the time thresholds of IR perturbations that a cell can tolerate maximally under different IR perturbation circumstances.
publisher Public Library of Science
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153456/
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