Xpa knockout mice

被引:22
作者
deVries, A
vanSteeg, H
机构
[1] Department of Carcinogenesis, Mutagenesis and Genetics, Natl. Inst. of Pub. Hlth. and E., 3720 BA Bilthoven
关键词
carcinogenesis; DNA repair; mutagenesis; photosensitivity; xeroderma pigmentosum;
D O I
10.1006/scbi.1996.0031
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The xeroderma pigmentosum group A correcting (XPA) gene encodes a DNA binding zinc-finger protein that recognizes DNA damage. As such the XPA protein participates in the initial step of the process of nucleotide excision repair: The multicomponent nucleotide excision repair pathway is one of the mast thoroughly studied mechanisms that defends both eukaryotic and prokaryotic cells against the deleterious effects of W-B and several chemical components. In the absence of nucleotide excision repair common cellular processes like transcription and replication are disturbed by persisting (unrepaired) DNA lesions (adducts), which may lead to the accumulation of gene mutations and ultimately to cancer Xeroderma pigmentosum patients have a >2000 fold increased risk to develop skin cancer at sun-exposed areas. Here we describe that XPA-deficient transgenic mice show features that mimic the phenotype found in humans. Furthermore, the possible use of Xpa- and other nucleotide excision repair deficient mice in cancer research will be outlined in more detail.
引用
收藏
页码:229 / 240
页数:12
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