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Increased susceptibility to ultraviolet-B and carcinogens of mice lacking the DNA excision repair gene XPA
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Increased susceptibility to ultraviolet-B and carcinogens of mice lacking the DNA excision repair gene XPA
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Journal Article
Increased susceptibility to ultraviolet-B and carcinogens of mice lacking the DNA excision repair gene XPA
1995
Overview
XERODERM A pigmentosum patients with a defect in the nucleotide-excision repair gene XPA are characterized by, for example, a > 1,000-fold higher risk of developing sunlight-induced skin cancer
1–3
. Nucleo tide-excision repair (NER) is involved in the removal of a wide spectrum of DNA lesions. The XPA protein functions in a pre-incision step, the recognition of DNA damage
4–7
. To permit the functional analysis of the XPA gene in vivo, we have generated
XPA
-deficient mice by gene targeting in embryonic stem cells. The
XPA
−f− mice appear normal, at least until the age of 13 months. XPA−1− mice are highly susceptible to ultraviolet (UV)-B-induced skin and eye tumours and to 7,12-dimethylbenz-[a]anthracene (DMBA)-induced skin tumours. We conclude that the
XPA
-deficient mice strongly mimic the phenotype of humans with xeroderma pigmentosum.
Publisher
Nature Publishing Group UK,Nature Publishing,Nature Publishing Group
Subject
9,10-Dimethyl-1,2-benzanthracene - toxicity
/ Animals
/ Biological and medical sciences
/ Classical genetics, quantitative genetics, hybrids
/ DNA
/ DNA-Binding Proteins - genetics
/ Eye Neoplasms - chemically induced
/ Fundamental and applied biological sciences. Psychology
/ Genetic Predisposition to Disease
/ Genetics
/ Genetics of eukaryotes. Biological and molecular evolution
/ Humanities and Social Sciences
/ Humans
/ letter
/ Mice
/ Neoplasms, Radiation-Induced - genetics
/ Rodents
/ Science
/ Skin Neoplasms - chemically induced
