ArticleProceedings of the National Academy of Sciences of the United States of America2023
Naturally mutagenic sequence diversity in a human type II topoisomerase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A multispecies toolkit ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Supercoiled DNA recognition and cleavage control in topoisomerase VI.Nature communications · 2026Article
- Structural Mechanisms of Topoisomerase-Targeting Drugs.Annual review of biochemistry · 2025Review
- Dynamic crosstalk between amino acid metabolism and cancer drug efficacy: From mechanisms to therapeutic opportunities.iScience · 2025Review
- Yeast Tools for Studying Type II Topoisomerases in Budding Yeast.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Genome Instability Induced by Topoisomerase Misfunction.International journal of molecular sciences · 2024Review
- Modeling allosteric mechanisms of eukaryotic type II topoisomerases.Biophysical journal · 2024Article
- Using energy to go downhill-a genoprotective role for ATPase activity in DNA topoisomerase II.Nucleic acids research · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Type II topoisomerases transiently cleave duplex DNA as part of a strand passage mechanism that helps control chromosomal organization and superstructure. Aberrant DNA cleavage can result in genomic instability, and how topoisomerase activity is controlled to prevent unwanted breaks is poorly understood. Using a genetic screen, we identified mutations in the beta isoform of human topoisomerase II (hTOP2β) that render the enzyme hypersensitive to the chemotherapeutic agent etoposide. Several of these variants were unexpectedly found to display hypercleavage behavior in vitro and to be capable of inducing cell lethality in a DNA repair-deficient background; surprisingly, a subset of these mutations were also observed in
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