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Cell cycle-dependent regulation of excision repair of UV damage.

Authors
  • Downes, C S
  • Johnson, R T
  • Collins, A R
Type
Published Article
Journal
Experimental cell research
Publication Date
Nov 01, 1982
Volume
142
Issue
1
Pages
47–56
Identifiers
PMID: 6754399
Source
Medline
License
Unknown

Abstract

The incision step of excision repair of UV-damaged DNA, represented by the accumulation of DNA strand breaks in the presence of hydroxyurea and 1-beta-D-arabinofuranosylcytosine, was measured in cultured cells of Microtus agrestis during quiescence and at different times after release from quiescence. The UV dose-dependent kinetics of enzymic incision change rapidly through the first cell cycle after release, with a maximum potential for enzymic incision and a minimum affinity of the incision system for damage sites occurring in late G1. The potential for incision falls to a lower level as cells approach a randomly proliferating state, whilst the affinity rises. Incision activity declines rapidly after UV irradiation, leaving many damage sites unrepaired; the enhanced survival seen in cells held in quiescence after irradiation is thus partly due to some other repair mode.

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