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pubmed-article:3627144pubmed:abstractTextThe limited DNA excision repair that occurs in the chromatin of UV-irradiated growth arrested cells isolated from a xeroderma pigmentosum (XP) complementation group C patient is clustered in localized regions. The repaired DNA was found to be more sensitive to nicking by endogenous nucleases than the bulk of the DNA. The extra-sensitivity does not change with increasing amounts of DNA damage or repair activity in the locally-repaired regions and is retained through a 24-h chase period. We suggest that these results are due to the occurrence of DNA repair limited to pre-existing, non-transient chromatin fractions that contain actively transcribed DNA. A similar extra-sensitivity of repaired DNA was not detected in cells of normal or XP complementation group A strains that exhibit either normal or limited repair located randomly throughout their genomes. The association between endogenous nuclease sensitivity and clustered repair probably defines a normal excision repair pathway that is specific for selected chromatin domains. The repair defect in XP-C strains may be one in pathways targeted for other endogenous nuclease-resistant domains.lld:pubmed
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pubmed-article:3627144pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:3627144pubmed:year1987lld:pubmed
pubmed-article:3627144pubmed:articleTitleThe endogenous nuclease sensitivity of repaired DNA in human fibroblasts.lld:pubmed
pubmed-article:3627144pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3627144pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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