ArticleNucleic acids research2006
Linking uracil base excision repair and 5-fluorouracil toxicity in yeast.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- The Molecular and Functional Landscape of Resistance to FOLFIRI Chemotherapy in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Advances and challenges in non-canonical nucleic acids data storage.Nature communications · 2026Review
- Mutation and Microsatellite Instability (MSI) Affect the Differential Gene Expression of Folic Acid and 5-Flourouracil Metabolism-Related Genes in Colorectal Carcinoma.Current oncology (Toronto, Ont.) · 2025Article
- Replication Protein A Enhances Kinetics of Uracil DNA Glycosylase on ssDNA and Across DNA Junctions: Explored with a DNA Repair Complex Produced with SpyCatcher/SpyTag Ligation.Chembiochem : a European journal of chemical biology · 2023Article
- Reproductive and developmental toxicities of 5-fluorouracil in model organisms and humans.Expert reviews in molecular medicine · 2022Review
- An efficient transformation system for Trichoderma atroviride using the pyr4 gene as a selectable marker.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2020Article
- Dietary serine-microbiota interaction enhances chemotherapeutic toxicity without altering drug conversion.Nature communications · 2020Article
- A robust photoluminescence screening assay identifies uracil-DNA glycosylase inhibitors against prostate cancer.Chemical science · 2020Article
- Inactivation of folylpolyglutamate synthetase Met7 results in genome instability driven by an increased dUTP/dTTP ratio.Nucleic acids research · 2020Article
- The Ca-loop in thymidylate kinase is critical for growth and contributes to pyrimidine drug sensitivity ofThe Journal of biological chemistry · 2019Article
- The anti-cancer drug 5-fluorouracil affects cell cycle regulators and potential regulatory long non-coding RNAs in yeast.RNA biology · 2019Article
- Improved Radiotherapy Sensitivity of Nasopharyngeal Carcinoma Cells by miR-29-3p Targeting COL1A1 3'-UTR.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The fitness cost and benefit of phase-separated protein deposits.Molecular systems biology · 2019Article
- The etiology of uracil residues in the Saccharomyces cerevisiae genomic DNA.Current genetics · 2019Review
- Sources of thymidine and analogs fueling futile damage-repair cycles and ss-gap accumulation during thymine starvation in Escherichia coli.DNA repair · 2019Article
- Nuclear Folate Metabolism.Annual review of nutrition · 2018Review
- Targeting nuclear thymidylate biosynthesis.Molecular aspects of medicine · 2017Review
- DCTPP1 attenuates the sensitivity of human gastric cancer cells to 5-fluorouracil by up-regulating MDR1 expression epigenetically.Oncotarget · 2016Article
- The applications of the novel polymeric fluoropyrimidine F10 in cancer treatment: current evidence.Future oncology (London, England) · 2016Review
- Populations adapt to fluctuating selection using derived and ancestral allelic diversity.Evolution; international journal of organic evolution · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
5-fluorouracil (5-FU) is a widely used anticancer drug that disrupts pyrimidine nucleotide pool balances and leads to uracil incorporation in DNA, which is then recognized and removed by the uracil base excision repair (BER) pathway. Using complementary biochemical and genetic approaches we have examined the role of uracil BER in the cell killing mechanism of 5-FU. A yeast strain lacking the enzyme uracil DNA glycosylase (Ung1), which excises uracil from the DNA backbone leaving an abasic site, showed significant protection against the toxic effects of 5-FU, a G1/S cell cycle arrest phenotype, and accumulated massive amounts of U/A base pairs in its genome (approximately 4% of T/A pairs were now U/A). A strain lacking the major abasic site endonuclease of Saccharomyces cerevisiae (Apn1) showed significantly increased sensitivity to 5-FU with G2/M arrest. Thus, efficient processing of abasic sites by this enzyme is protective against the toxic effects of 5-FU. However, contrary to expectations, the Apn1 deficient strain did not accumulate intact abasic sites, indicating that another repair pathway attempts to process these sites in the absence Apn1, but that this process has catastrophic effects on genome integrity. These findings suggest that new strategies for chemical intervention targeting BER could enhance the effectiveness of this widely used anticancer drug.
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