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基于动力学理论的基因组应激下细胞修复机制建模方法。

Kinetic theory approach to modeling of cellular repair mechanisms under genome stress.

机构信息

College of Information Science and Technology, Donghua University, Shanghai, People's Republic of China.

出版信息

PLoS One. 2011;6(8):e22228. doi: 10.1371/journal.pone.0022228. Epub 2011 Aug 9.

DOI:10.1371/journal.pone.0022228
PMID:21857915
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3153456/
Abstract

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.

摘要

在外部环境的剧烈干扰下，正常细胞可以触发细胞自身防御机制，以应对基因组压力。为了进一步研究单细胞水平上细胞自我修复过程的动力学，我们使用活性粒子动力理论（KTAP）的数学框架，提出了一种在急性离子辐射（IR）下产生和修复 DNA 损伤的模型。首先，我们专注于说明由两个亚群组成的细胞修复系统（CRS）的概况，每个亚群由具有不同离散状态的活性粒子组成。然后，我们实现了细胞自我修复机制的数学框架，并说明了双链断裂（DSBs）和修复蛋白（RP）产生、DSB-蛋白复合物（DSBCs）合成和毒素积累的动态过程。最后，我们粗略分析了细胞自我修复机制的能力、细胞转移 DNA 损伤的活性和基因组稳定性，特别是在不同 IR 干扰情况下细胞可以最大耐受的 IR 干扰时间阈值前后，某个细胞的不同命运。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/e7f9d4574064/pone.0022228.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/6b7461845159/pone.0022228.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/35dc02a3631a/pone.0022228.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/4725d24d6b24/pone.0022228.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/3265603f2e65/pone.0022228.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/8d492cbb7885/pone.0022228.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/42631505653d/pone.0022228.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/a1223541dfc5/pone.0022228.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/e1ace85f500e/pone.0022228.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/e7f9d4574064/pone.0022228.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/6b7461845159/pone.0022228.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/35dc02a3631a/pone.0022228.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/4725d24d6b24/pone.0022228.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/3265603f2e65/pone.0022228.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/8d492cbb7885/pone.0022228.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/42631505653d/pone.0022228.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/a1223541dfc5/pone.0022228.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/e1ace85f500e/pone.0022228.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55b1/3153456/e7f9d4574064/pone.0022228.g009.jpg

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2
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Curr Top Dev Biol. 2008;81:485-502. doi: 10.1016/S0070-2153(07)81017-9.
3
A mathematical model of P53 gene regulatory networks under radiotherapy.
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4
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Amino Acids. 2007 Jul;33(1):75-83. doi: 10.1007/s00726-006-0454-3. Epub 2006 Oct 31.
5
A plausible model for the digital response of p53 to DNA damage.一种关于p53对DNA损伤的数字反应的合理模型。
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6
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Biochem Biophys Res Commun. 2005 Aug 26;334(2):386-94. doi: 10.1016/j.bbrc.2005.06.097.
7
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Biochem Biophys Res Commun. 2005 Jun 10;331(3):816-27. doi: 10.1016/j.bbrc.2005.03.186.
8
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9
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