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本文引用的文献

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A non-heme iron-mediated chemical demethylation in DNA and RNA.非血红素铁介导的 DNA 和 RNA 化学去甲基化。
Acc Chem Res. 2009 Apr 21;42(4):519-29. doi: 10.1021/ar800178j.
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Recognition and processing of a new repertoire of DNA substrates by human 3-methyladenine DNA glycosylase (AAG).人类3-甲基腺嘌呤DNA糖基化酶(AAG)对新的DNA底物文库的识别与处理
Biochemistry. 2009 Mar 10;48(9):1850-61. doi: 10.1021/bi8018898.
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Stochastic properties of processive cytidine DNA deaminases AID and APOBEC3G.连续性胞嘧啶DNA脱氨酶AID和APOBEC3G的随机特性。
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Oxidative demethylation of 3-methylthymine and 3-methyluracil in single-stranded DNA and RNA by mouse and human FTO.小鼠和人类FTO对单链DNA和RNA中3-甲基胸腺嘧啶和3-甲基尿嘧啶的氧化去甲基化作用。
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Advances in chemical carcinogenesis: a historical review and prospective.化学致癌作用的进展:历史回顾与展望
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The AID/APOBEC family of nucleic acid mutators.AID/APOBEC核酸突变酶家族。
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Cancers exhibit a mutator phenotype: clinical implications.癌症呈现出突变体表型:临床意义。
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Oxidative stress, DNA methylation and carcinogenesis.氧化应激、DNA甲基化与致癌作用。
Cancer Lett. 2008 Jul 18;266(1):6-11. doi: 10.1016/j.canlet.2008.02.026. Epub 2008 Mar 26.
9
Beyond aerobic glycolysis: transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis.超越有氧糖酵解:转化细胞可进行超过蛋白质和核苷酸合成所需的谷氨酰胺代谢。
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The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.与肥胖相关的FTO基因编码一种依赖于2-氧戊二酸的核酸去甲基化酶。
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诱变和 DNA 修复的化学生物学:细胞对 DNA 烷化的反应。

Chemical biology of mutagenesis and DNA repair: cellular responses to DNA alkylation.

机构信息

Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

出版信息

Carcinogenesis. 2010 Jan;31(1):59-70. doi: 10.1093/carcin/bgp262. Epub 2009 Oct 29.

DOI:10.1093/carcin/bgp262
PMID:19875697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2802671/
Abstract

The reaction of DNA-damaging agents with the genome results in a plethora of lesions, commonly referred to as adducts. Adducts may cause DNA to mutate, they may represent the chemical precursors of lethal events and they can disrupt expression of genes. Determination of which adduct is responsible for each of these biological endpoints is difficult, but this task has been accomplished for some carcinogenic DNA-damaging agents. Here, we describe the respective contributions of specific DNA lesions to the biological effects of low molecular weight alkylating agents.

摘要

DNA 损伤剂与基因组的反应会导致大量损伤,通常称为加合物。加合物可能导致 DNA 突变,它们可能是致命事件的化学前体,也可能破坏基因的表达。确定哪种加合物负责这些生物学终点中的每一个是困难的,但对于一些致癌 DNA 损伤剂已经完成了这项任务。在这里,我们描述了特定 DNA 损伤对低分子量烷化剂生物效应的各自贡献。