ArticleProceedings of the National Academy of Sciences of the United States of America2003
Endonuclease cleavage of blocked replication forks: An indirect pathway of DNA damage from antitumor drug-topoisomerase complexes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Our Evolving Understanding of the Mechanism of Quinolones.Antibiotics (Basel, Switzerland) · 2018Review
- Functions that protect Escherichia coli from DNA-protein crosslinks.DNA repair · 2015Article
- SbcCD-mediated processing of covalent gyrase-DNA complex in Escherichia coli.Antimicrobial agents and chemotherapy · 2013Article
- MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA.Biology open · 2012Article
- Use of RecA fusion proteins to induce genomic modifications in zebrafish.Nucleic acids research · 2011Article
- Initiation of bacteriophage T4 DNA replication and replication fork dynamics: a review in the Virology Journal series on bacteriophage T4 and its relatives.Virology journal · 2010Review
- Rescue of bacteriophage T7 DNA polymerase of low processivity by suppressor mutations affecting gene 3 endonuclease.Journal of virology · 2009Article
- Cleavage of a model DNA replication fork by a Type I restriction endonuclease.Nucleic acids research · 2009Article
- Quinolones: action and resistance updated.Current topics in medicinal chemistry · 2009Review
- The epsilon subunit of DNA polymerase III Is involved in the nalidixic acid-induced SOS response in Escherichia coli.Journal of bacteriology · 2008Article
- Regression supports two mechanisms of fork processing in phage T4.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Quinolone-mediated bacterial death.Antimicrobial agents and chemotherapy · 2008Review
- Genetic analysis of the requirements for SOS induction by nalidixic acid in Escherichia coli.Gene · 2005Article
- Norfloxacin-induced DNA gyrase cleavage complexes block Escherichia coli replication forks, causing double-stranded breaks in vivo.Molecular microbiology · 2005Article
- Isolation of SOS constitutive mutants of Escherichia coli.Journal of bacteriology · 2004Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The cytotoxicity of several important antitumor drugs depends on formation of the covalent topoisomerase-DNA cleavage complex. However, cellular processes such as DNA replication are necessary to convert the cleavage complex into a cytotoxic lesion, but the molecular mechanism of this conversion and the precise nature of the cytotoxic lesion are unknown. Using a bacteriophage T4 model system, we have previously shown that antitumor drug-induced cleavage complexes block replication forks in vivo. In this report, we show that these blocked forks can be cleaved by T4 endonuclease VII to create overt DNA breaks. The accumulation of blocked forks increased in endonuclease VII-deficient infections, suggesting that endonuclease cleavage contributes to fork processing in vivo. Furthermore, purified endonuclease VII cleaved the blocked forks in vitro close to the branch points. These results suggest that an indirect pathway of branched-DNA cleavage contributes to the cytotoxicity of antitumor drugs that target DNA topoisomerases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.