Abstract: 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 most thoroughly studied mechanisms that defends both eukaryotic and prokaryotic cells against the deleterious effects of UV-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 thatXpa-deficient transgenic mice show features that mimic the phenotype found in humans. Furthermore, the possible use ofXpa- and other nucleotide excision repair deficient mice in cancer research will be outlined in more detail.
Publication Year: 1996
Publication Date: 1996-10-01
Language: en
Type: review
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 29
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