Correlation of Post-UV Colony-Forming Abilities of Xeroderma Pigmentosum Fibroblasts with DNA Incision Reactions Catalyzed by Cell-Free Extracts
Xeroderma pigmentosum is an autosomal recessive genodermatosis which is characterized by abnormal dryness, atrophy, pigmentation abnormalities, and early carcinomas of the skin if exposed to sunlight (1). Cultivated XP fibroblasts show lower levels of DNA excision repair after exposure to UV irradiation or UV-like carcinogens such as (Ac)2 ONFln. There are currently 7 excision repair-deficient forms, classified as complementation groups A-G (2), which suggests that several gene products are involved in excision repair of UV-damaged DNA. It seems generally accepted that XP cells of all complementation groups are defective at the level of DNA incision (2,3). However, our knowledge regarding the precise enzymic deficiency by which a particular complementation group is characterized is still incomplete.
- UV light
- AP sites
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- 1.J. M. Mascaró, Xeroderma pigmentosum, in: Cancer of the skin, Vol. 1, R. Andrade, S. L. Gumport, G. L. Popkin, T. D. Rees (eds.), pp. 573–595, W. B. Saunders Co., Philadelphia, London, Toronto (1976).Google Scholar