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. 1982 Sep 11;10(17):5357–5368. doi: 10.1093/nar/10.17.5357

Effects of DNA replication inhibitors on UV excision repair in synchronised human cells.

C S Downes, A R Collins
PMCID: PMC320877  PMID: 7145704

Abstract

When HeLa cells are irradiated with UV and treated with the DNA synthesis inhibitors hydroxyurea (HU) and 1-beta-D-arabinofuranosylcytosine (ara C), DNA strand breaks accumulate at sites where excision repair of DNA damage has been inhibited after the incision step. This break accumulation occurs in mitotic, G1 and S phase cells. But UV-induced repair synthesis of DNA, as measured by [3H]thymidine incorporation into unreplicated DNA, is not inhibited by HU and ara C in G1 or S phase cells, even though replicative synthesis is virtually abolished. Repair and replication must therefore utilise different DNA precursor pools, or different DNA synthetic systems; and the action of Hu and ara C in causing strand break accumulation may occur at the ligation step of excision repair.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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