Genomically Incorporated 5-Fluorouracil that Escapes UNG-Initiated Base Excision Repair Blocks DNA Replication and Activates Homologous Recombination
about
Inhibition of uracil DNA glycosylase sensitizes cancer cells to 5-fluorodeoxyuridine through replication fork collapse-induced DNA damage.Glycogen Synthase Kinase 3 (GSK-3)-mediated Phosphorylation of Uracil N-Glycosylase 2 (UNG2) Facilitates the Repair of Floxuridine-induced DNA Lesions and Promotes Cell Survival.Targeting nuclear thymidylate biosynthesis.dUTPase inhibition augments replication defects of 5-Fluorouracil.Assessment of metabolism-dependent drug efficacy and toxicity on a multilayer organs-on-a-chip.
P2860
Genomically Incorporated 5-Fluorouracil that Escapes UNG-Initiated Base Excision Repair Blocks DNA Replication and Activates Homologous Recombination
description
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name
Genomically Incorporated 5-Flu ...... vates Homologous Recombination
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Genomically Incorporated 5-Flu ...... vates Homologous Recombination
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type
label
Genomically Incorporated 5-Flu ...... vates Homologous Recombination
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Genomically Incorporated 5-Flu ...... vates Homologous Recombination
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prefLabel
Genomically Incorporated 5-Flu ...... vates Homologous Recombination
@ast
Genomically Incorporated 5-Flu ...... vates Homologous Recombination
@en
P2093
P2860
P356
P1476
Genomically Incorporated 5-Flu ...... vates Homologous Recombination
@en
P2093
Amelia M Huehls
Carly A Baehr
Catherine J Huntoon
Jill M Wagner
Larry M Karnitz
Marietta Y Lee
Xiaoxiao Wang
P2860
P356
10.1124/MOL.115.100164
P577
2015-10-22T00:00:00Z