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DNA 错配修复依赖性 DNA 损伤反应与癌症。

DNA mismatch repair-dependent DNA damage responses and cancer.

机构信息

Department of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands.

Department of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands.

出版信息

DNA Repair (Amst). 2020 Sep;93:102923. doi: 10.1016/j.dnarep.2020.102923.

DOI:10.1016/j.dnarep.2020.102923
PMID:33087264
Abstract

Canonical DNA mismatch repair (MMR) excises base-base mismatches to increase the fidelity of DNA replication. Thus, loss of MMR leads to increased spontaneous mutagenesis. MMR genes also are involved in the suppression of mutagenic, and the induction of protective, responses to various types of DNA damage. In this review we describe these non-canonical roles of MMR at different lesion types. Loss of non-canonical MMR gene functions may have important ramifications for the prevention, development and treatment of colorectal cancer associated with inherited MMR gene defects in Lynch syndrome. This graphical review pays tribute to Samuel H. Wilson. Sam not only made seminal contributions to understanding base excision repair, particularly with respect to structure-function relationships in DNA polymerase β but also, as Editor of DNA Repair, has maintained a high standard of the journal.

摘要

经典的 DNA 错配修复(MMR)切除碱基对错配以提高 DNA 复制的保真度。因此,MMR 的缺失会导致自发突变率增加。MMR 基因还参与抑制诱变和诱导对各种类型 DNA 损伤的保护性反应。在这篇综述中,我们描述了 MMR 在不同损伤类型下的这些非经典作用。非经典 MMR 基因功能的丧失可能对预防、发展和治疗与林奇综合征中遗传 MMR 基因缺陷相关的结直肠癌产生重要影响。这篇图文并茂的综述是为了纪念塞缪尔·H·威尔逊(Samuel H. Wilson)。山姆不仅对理解碱基切除修复做出了开创性的贡献,特别是在 DNA 聚合酶β的结构-功能关系方面,而且作为 DNA 修复的编辑,他还保持了该杂志的高标准。

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