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Defective postreplication repair in xeroderma pigmentosum variant fibroblasts
1990
Cancer Research
Postreplication repair (PRR) was quantified in normal human fibroblasts and in xeroderma pigmentosum (XP) variant fibroblasts after treatment with UV or benzo[a]pyrene diol epoxide-I (BPDE-I). PRR may be defined as the elimination of discontinuities in the daughter-strand DNA and the replicative bypass of lesions in the DNA template. Pathways of PRR reduce the number of DNA growing points that are blocked at template lesions and increase the rate of growth of nascent DNA on damaged templates.
pmid:2109654
fatcat:ggv7kdk3yra4jbd26ax6o6bfk4