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通过体外试验监测碱基切除修复。

Monitoring base excision repair by in vitro assays.

作者信息

Dianov Grigory L

机构信息

MRC Radiation and Genome Stability Unit, Medical Research Council, Harwell, OX11 0RD Oxfordshire, UK.

出版信息

Toxicology. 2003 Nov 15;193(1-2):35-41. doi: 10.1016/s0300-483x(03)00288-9.

DOI:10.1016/s0300-483x(03)00288-9
PMID:14599766
Abstract

Base excision repair (BER) is the major mechanism for processing of mutagenic and genotoxic DNA base lesions caused by cellular environmental or exogenous mutagens. In vitro base excision repair assays have been used in studies aimed at understanding the nature of various human diseases, aging and mechanisms of genome recovery after mutagenic stress. This review describes the key base excision repair assays and addresses their advantages and limitations.

摘要

碱基切除修复（BER）是处理由细胞环境或外源性诱变剂引起的诱变和基因毒性DNA碱基损伤的主要机制。体外碱基切除修复分析已用于旨在了解各种人类疾病的本质、衰老以及诱变应激后基因组恢复机制的研究中。本综述描述了关键的碱基切除修复分析，并阐述了它们的优点和局限性。

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Templated chemistry for monitoring damage and repair directly in duplex DNA.
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Uracil-DNA glycosylase of Thermoplasma acidophilum directs long-patch base excision repair, which is promoted by deoxynucleoside triphosphates and ATP/ADP, into short-patch repair.嗜热酸原体的尿嘧啶-DNA 糖基化酶将长补丁碱基切除修复引导为短补丁修复，该修复过程由脱氧核苷三磷酸和 ATP/ADP 促进。
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