5-Fluorouracil incorporated into DNA is excised by the Smug1 DNA glycosylase to reduce drug cytotoxicity.
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DNA mismatch repair: molecular mechanism, cancer, and ageingDNA glycosylases: in DNA repair and beyondOverview of base excision repair biochemistryBase excision by thymine DNA glycosylase mediates DNA-directed cytotoxicity of 5-fluorouracilFluoropyrimidine ActivityExcision of 5-halogenated uracils by human thymine DNA glycosylase. Robust activity for DNA contexts other than CpG.The effect of Pot1 binding on the repair of thymine analogs in a telomeric DNA sequenceCheckpoint signaling, base excision repair, and PARP promote survival of colon cancer cells treated with 5-fluorodeoxyuridine but not 5-fluorouracil.SMUG1 but not UNG DNA glycosylase contributes to the cellular response to recovery from 5-fluorouracil induced replication stressSingle-strand selective monofunctional uracil-DNA glycosylase (SMUG1) deficiency is linked to aggressive breast cancer and predicts response to adjuvant therapy.Effect of the thymidylate synthase inhibitors on dUTP and TTP pool levels and the activities of DNA repair glycosylases on uracil and 5-fluorouracil in DNA.Uracil-DNA glycosylase in base excision repair and adaptive immunity: species differences between man and mouse.Synergistic enhancement of 5-fluorouracil cytotoxicity by deoxyuridine analogs in cancer cells.UNG-initiated base excision repair is the major repair route for 5-fluorouracil in DNA, but 5-fluorouracil cytotoxicity depends mainly on RNA incorporation.Exploiting base excision repair to improve therapeutic approaches for pancreatic cancerHigh mobility group protein B1 is an activator of apoptotic response to antimetabolite drugs.Genomically Incorporated 5-Fluorouracil that Escapes UNG-Initiated Base Excision Repair Blocks DNA Replication and Activates Homologous RecombinationPredictive markers for the response to 5-fluorouracil therapy in cancer cells: Constant-field gel electrophoresis as a tool for prediction of response to 5-fluorouracil-based chemotherapy.DNA mismatch repair and the DNA damage response.5-Fluorouracil mediated anti-cancer activity in colon cancer cells is through the induction of Adenomatous Polyposis Coli: Implication of the long-patch base excision repair pathway.Base excision repair, aging and health span.The mismatch repair-mediated cell cycle checkpoint response to fluorodeoxyuridine.Genetic variants in DNA repair pathway genes and risk of esophageal squamous cell carcinoma and gastric adenocarcinoma in a Chinese populationFolate deficiency induces genomic uracil misincorporation and hypomethylation but does not increase DNA point mutations.Establishing a model for assessing DNA damage in murine brain cells as a molecular marker of chemotherapy-associated cognitive impairment.Participation of DNA repair in the response to 5-fluorouracil.Uracil in DNA: consequences for carcinogenesis and chemotherapy5-Fluorouracil: mechanisms of resistance and reversal strategies.Small interfering RNA-directed knockdown of uracil DNA glycosylase induces apoptosis and sensitizes human prostate cancer cells to genotoxic stress.Impairment of APE1 function enhances cellular sensitivity to clinically relevant alkylators and antimetabolites.Inhibition of uracil DNA glycosylase sensitizes cancer cells to 5-fluorodeoxyuridine through replication fork collapse-induced DNA damage.DNA damage and repair in human cancer: molecular mechanisms and contribution to therapy-related leukemias.My journey to DNA repair.Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.TAS-102, a novel antitumor agent: a review of the mechanism of action.Conserved molecular mechanisms underlying the effects of small molecule xenobiotic chemotherapeutics on cells.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.The applications of the novel polymeric fluoropyrimidine F10 in cancer treatment: current evidence.Cellular response to efficient dUTPase RNAi silencing in stable HeLa cell lines perturbs expression levels of genes involved in thymidylate metabolism.Novel opportunities for thymidylate metabolism as a therapeutic target.
P2860
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P2860
5-Fluorouracil incorporated into DNA is excised by the Smug1 DNA glycosylase to reduce drug cytotoxicity.
description
2007 nî lūn-bûn
@nan
2007 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@ast
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@en
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@nl
type
label
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@ast
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@en
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@nl
altLabel
5-Fluorouracil incorporated in ...... se to reduce drug cytotoxicity
@en
prefLabel
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@ast
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@en
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@nl
P2093
P1433
P1476
5-Fluorouracil incorporated in ...... e to reduce drug cytotoxicity.
@en
P2093
Deborah E Barnes
Peter Robins
P356
10.1158/0008-5472.CAN-06-2960
P407
P577
2007-02-01T00:00:00Z