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XB-ART-15035
J Biol Chem 1998 Apr 10;27315:8842-8.
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Involvement of flap endonuclease 1 in base excision DNA repair.

Kim K , Biade S , Matsumoto Y .


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Base excision repair can proceed in either one of two alternative pathways: a DNA polymerase beta-dependent pathway and a proliferating cell nuclear antigen (PCNA)-dependent pathway. Excision of an apurinic/apyrimidinic (AP) site by cutting the phosphate backbone on its 3' side following incision at its 5' side by AP endonuclease is a prerequisite to completion of these repair pathways. Using a reconstituted system with the proteins derived from Xenopus laevis, we found that flap endonuclease 1 (FEN1) was a factor responsible for the excision of a 5'-incised AP site in the PCNA-dependent pathway. In this pathway, DNA synthesis was not required for the action of FEN1 in the presence of PCNA and a replication factor C-containing fraction. The polymerase beta-dependent pathway could also use FEN1 for excision of the synthetic AP sites, which were not susceptible to beta-elimination. In this pathway, FEN1 was functional without PCNA and replication factor C but required the DNA synthesis, which led to a flap structure formation.

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Species referenced: Xenopus laevis
Genes referenced: fen1 pcna