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本文引用的文献

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Recruitment of DNA damage checkpoint proteins to damage in transcribed and nontranscribed sequences.将DNA损伤检查点蛋白招募至转录和非转录序列中的损伤处。
Mol Cell Biol. 2006 Jan;26(1):39-49. doi: 10.1128/MCB.26.1.39-49.2006.
2
Mathematical modeling of nucleotide excision repair reveals efficiency of sequential assembly strategies.核苷酸切除修复的数学模型揭示了顺序组装策略的效率。
Mol Cell. 2005 Sep 2;19(5):679-90. doi: 10.1016/j.molcel.2005.06.036.
3
Molecular mechanisms of mammalian DNA repair and the DNA damage checkpoints.哺乳动物DNA修复及DNA损伤检查点的分子机制。
Annu Rev Biochem. 2004;73:39-85. doi: 10.1146/annurev.biochem.73.011303.073723.
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Thermodynamic cooperativity and kinetic proofreading in DNA damage recognition and repair.DNA损伤识别与修复中的热力学协同性和动力学校对
Cell Cycle. 2004 Feb;3(2):141-4.
5
Recognition and repair of the cyclobutane thymine dimer, a major cause of skin cancers, by the human excision nuclease.人类切除核酸酶对环丁烷胸腺嘧啶二聚体（皮肤癌的主要病因）的识别与修复。
Genes Dev. 2003 Oct 15;17(20):2539-51. doi: 10.1101/gad.1131003. Epub 2003 Oct 1.
6
The SWI/SNF chromatin-remodeling factor stimulates repair by human excision nuclease in the mononucleosome core particle.SWI/SNF染色质重塑因子可刺激人切除核酸酶对单核小体核心颗粒进行修复。
Mol Cell Biol. 2002 Oct;22(19):6779-87. doi: 10.1128/MCB.22.19.6779-6787.2002.
7
Molecular anatomy of the human excision nuclease assembled at sites of DNA damage.在DNA损伤位点组装的人类切除核酸酶的分子解剖学。
Mol Cell Biol. 2002 Aug;22(16):5938-45. doi: 10.1128/MCB.22.16.5938-5945.2002.
8
The XPC-HR23B complex displays high affinity and specificity for damaged DNA in a true-equilibrium fluorescence assay.在真实平衡荧光测定中，XPC-HR23B复合物对受损DNA表现出高亲和力和特异性。
Biochemistry. 2002 May 28;41(21):6583-7. doi: 10.1021/bi012202t.
9
Sequential assembly of the nucleotide excision repair factors in vivo.核苷酸切除修复因子在体内的顺序组装。
Mol Cell. 2001 Jul;8(1):213-24. doi: 10.1016/s1097-2765(01)00281-7.
10
DNA repair excision nuclease attacks undamaged DNA. A potential source of spontaneous mutations.DNA修复切除核酸酶会攻击未受损的DNA。这是自发突变的一个潜在来源。
J Biol Chem. 2001 Jul 6;276(27):25421-6. doi: 10.1074/jbc.M101032200. Epub 2001 May 15.

人类核苷酸切除修复的数学模型：通过随机顺序组装和动力学校对进行损伤识别。

A mathematical model for human nucleotide excision repair: damage recognition by random order assembly and kinetic proofreading.

作者信息

Kesseler Kevin J, Kaufmann William K, Reardon Joyce T, Elston Timothy C, Sancar Aziz

机构信息

Department of Pathology and Laboratory Medicine, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7255, USA.

出版信息

J Theor Biol. 2007 Nov 21;249(2):361-75. doi: 10.1016/j.jtbi.2007.07.025. Epub 2007 Aug 8.

DOI:10.1016/j.jtbi.2007.07.025
PMID:17869273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2702209/
Abstract

A mathematical model of human nucleotide excision repair was constructed and validated. The model incorporates cooperative damage recognition by RPA, XPA, and XPC followed by three kinetic proofreading steps by the TFIIH transcription/repair factor. The model yields results consistent with experimental data regarding excision rates of UV photoproducts by the reconstituted human excision nuclease system as well as the excision of oligonucleotides from undamaged DNA. The model predicts the effect that changes in the initial concentrations of repair factors have on the excision rate of damaged DNA and provides a testable hypothesis on the biochemical mechanism of cooperativity in protein assembly, suggesting experiments to determine if cooperativity in protein assembly results from an increased association rate or a decreased dissociation rate. Finally, a comparison between the random order assembly with kinetic proofreading model and a sequential assembly model is made. This investigation reveals the advantages of the random order assembly/kinetic proofreading model.

摘要

构建并验证了人类核苷酸切除修复的数学模型。该模型纳入了RPA、XPA和XPC的协同损伤识别，随后是TFIIH转录/修复因子的三个动力学校对步骤。该模型得出的结果与关于重组人类切除核酸酶系统对紫外线光产物的切除率以及从未受损DNA中切除寡核苷酸的实验数据一致。该模型预测了修复因子初始浓度的变化对受损DNA切除率的影响，并为蛋白质组装中协同作用的生化机制提供了一个可检验的假设，建议进行实验以确定蛋白质组装中的协同作用是由缔合速率增加还是解离速率降低导致的。最后，对具有动力学校对模型的随机顺序组装和顺序组装模型进行了比较。这项研究揭示了随机顺序组装/动力学校对模型的优势。