INCREASED SUSCEPTIBILITY TO ULTRAVIOLET-B AND CARCINOGENS OF MICE LACKING THE DNA EXCISION-REPAIR GENE XPA

Citation
A. Devries et al., INCREASED SUSCEPTIBILITY TO ULTRAVIOLET-B AND CARCINOGENS OF MICE LACKING THE DNA EXCISION-REPAIR GENE XPA, Nature, 377(6545), 1995, pp. 169-173
Citations number
17
Categorie Soggetti
Multidisciplinary Sciences
Journal title
NatureACNP
ISSN journal
00280836
Volume
377
Issue
6545
Year of publication
1995
Pages
169 - 173
Database
ISI
SICI code
0028-0836(1995)377:6545<169:ISTUAC>2.0.ZU;2-Y
Abstract
XERODERMA pigmentosum patients with a defect in the nucleotide-excisio n repair gene XPA are characterized by, for example, a >1,000-fold hig her risk of developing sunlight-induced skin cancer(1-3). Nucleotide-e xcision repair (NER) is involved in the removal of a wide spectrum of DNA lesions, The XPA protein functions in a pre-incision step, the rec ognition of DNA damage(4-7). To permit tile functional analysis of the XPA gene in vivo, we have generated XPA-deficient mice by gene target ing in embryonic stem cells, The YPA(-/-) mice appear normal, at least until the age of 13 months, XPA(-/-) mice are highly susceptible to u ltraviolet (UV)-B-induced skin and eye tumours and to 7,12-dimethylben z[a]anthracene (DMBA)-induced skin tumours, We conclude that the XPA-d eficient mice strongly mimic the phenotype of humans with xeroderma pi gmentosum.