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• W1978265364 endingPage "15914" @default.
• W1978265364 startingPage "15903" @default.
• W1978265364 abstract "Recently, we found an interaction between adenomatous polyposis coli (APC) and DNA polymerase β (pol-β) and showed that APC blocks strand-displacement synthesis of long-patch base excision repair (LP-BER) (Narayan, S., Jaiswal, A. S., and Balusu, R. (2005) J. Biol. Chem. 280, 6942−6949); however, the mechanism is not clear. Using an in vivo LP-BER assay system, we now show that the LP-BER is higher in APC-/- cells than in APC+/+ cells. In addition to pol-β, the pull-down experiments showed that the full-length APC also interacted with flap endonuclease 1 (Fen-1). To further characterize the interaction of APC with pol-β and Fen-1, we performed a domain-mapping of APC and found that both pol-β and Fen-1 interact with a 138-amino acids peptide from the APC at the DRI-domain. Our functional assays showed that APC blocks pol-β-mediated 1-nucleotide (1-nt) as well as strand-displacement synthesis of reduced abasic, nicked-, or 1-nt gapped-DNA substrates. Further studies demonstrated that APC blocks 5‘-flap endonuclease as well as the 5‘−3‘ exonuclease activity of Fen-1 resulting in the blockage of LP-BER. From these results, we concluded that APC can have three different effects on the LP-BER pathway. First, APC can block pol-β-mediated 1-nt incorporation and strand-displacement synthesis. Second, APC can block LP-BER by blocking the coordinated formation and removal of the strand-displaced flap. Third, APC can block LP-BER by blocking hit-and-run synthesis. These studies will have important implications for APC in DNA damage-induced carcinogenesis and chemoprevention." @default.
• W1978265364 created "2016-06-24" @default.
• W1978265364 creator A5008820047 @default.
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• W1978265364 creator A5073212087 @default.
• W1978265364 date "2006-11-30" @default.
• W1978265364 modified "2023-10-17" @default.
• W1978265364 title "Mechanism of Adenomatous Polyposis Coli (APC)-Mediated Blockage of Long-Patch Base Excision Repair" @default.
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• W1978265364 doi "https://doi.org/10.1021/bi0607958" @default.
• W1978265364 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2528549" @default.
• W1978265364 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17176113" @default.
• W1978265364 hasPublicationYear "2006" @default.
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