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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2011
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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/ |
_version_ |
1611470151870316544 |