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首页> 外文期刊>Biochemistry >Nucleotide excision repair of 5-formyluracil in vitro is enhanced by the presence of mismatched bases.
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Nucleotide excision repair of 5-formyluracil in vitro is enhanced by the presence of mismatched bases.

机译：碱基错配的存在增强了5-甲酰尿嘧啶在体外的核苷酸切除修复。

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摘要

5-Formyluracil (fU) is a major thymine lesion produced by reactive oxygen radicals and photosensitized oxidation. Although this residue is a potentially mutagenic lesion and is removed by several base excision repair enzymes, it is unknown whether fU is the substrate of nucleotide excision repair (NER). Here, we analyzed the binding specificity of XPC-HR23B, which initiates NER, and cell-free NER activity on fU opposite four different bases. The result of the gel mobility shift assay showed that XPC-HR23B binds the fU-containing substrates in the following order: fU:C fU:T > fU:G > fU:A. Furthermore, in the presence of XPC-HR23B, the dual incision activity was the same as the order of the binding affinity of XPC-HR23B to fU. Therefore, it is concluded that even fU, regarded as a shape mimic of thymine, can be recognized as a substrate of NER incision, and the efficiency depends on instability of the base pair.
机译：5-甲酰尿嘧啶（fU）是一种主要的胸腺嘧啶损伤，由活性氧自由基和光敏氧化作用产生。尽管此残基是潜在的诱变性病变，并已被几种碱基切除修复酶清除，但尚不知道fU是否为核苷酸切除修复（NER）的底物。在这里，我们分析了XPC-HR23B的结合特异性，后者启动NER，并且在与四个不同碱基相对的fU上产生无细胞NER活性。凝胶迁移率变动分析的结果表明，XPC-HR23B按以下顺序结合含fU的底物：fU：C fU：T> fU：G> fU：A。此外，在XPC-HR23B的存在下，双重切口活性与XPC-HR23B对fU的结合亲和力的顺序相同。因此，可以得出结论，甚至认为fU（被视为胸腺嘧啶的形状模拟）也可以被视为NER切口的基质，并且效率取决于碱基对的不稳定性。

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