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烷基化诱变机制的模型。

A model for the mechanism of alkylation mutagenesis.

作者信息

Schendel P F, Michaeli I

出版信息

Mutat Res. 1984 Jan;125(1):1-14. doi: 10.1016/0027-5107(84)90026-5.

DOI:10.1016/0027-5107(84)90026-5
PMID:6690908
Abstract

The phenomenology of mutagenesis by N-methyl-N'-nitro-N-nitrosoguanidine and related alkylating agents is reviewed and a three-step model for the molecular events of mutagenesis is presented. The first step is the production of miscoding lesions, especially O6-methylguanine, and the induction and synthesis of methyltransferase. The second step is the generation of DNA sequences in which O6-methylguanine is paired with thymine. The third step is the conversion of this abnormal base pair to an adenine-thymine pair completing the production of a transition mutation. At each of these steps, factors which affect the ultimate mutation frequency are outlined. The model is then described formally and the limits of the model are discussed.

摘要

本文综述了N-甲基-N'-硝基-N-亚硝基胍及相关烷基化剂诱变的现象学,并提出了诱变分子事件的三步模型。第一步是产生错配损伤,特别是O6-甲基鸟嘌呤,以及甲基转移酶的诱导和合成。第二步是产生O6-甲基鸟嘌呤与胸腺嘧啶配对的DNA序列。第三步是将这种异常碱基对转化为腺嘌呤-胸腺嘧啶对,完成转换突变的产生。在这些步骤的每一步中,都概述了影响最终突变频率的因素。然后正式描述该模型,并讨论模型的局限性。

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1
A model for the mechanism of alkylation mutagenesis.烷基化诱变机制的模型。
Mutat Res. 1984 Jan;125(1):1-14. doi: 10.1016/0027-5107(84)90026-5.
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Defects in base excision repair combined with elevated intracellular dCTP levels dramatically reduce mutation induction in yeast by ethyl methanesulfonate and N-methyl-N'-nitro-N-nitrosoguanidine.碱基切除修复缺陷与细胞内dCTP水平升高相结合,可显著降低甲磺酸乙酯和N-甲基-N'-硝基-N-亚硝基胍对酵母的诱变作用。
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