ArticleProceedings of the National Academy of Sciences of the United States of America1999
CDC45 and DPB11 are required for processive DNA replication and resistance to DNA topoisomerase I-mediated DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 59 citations in OpenAlex.
- Chromenopyrimidinone Controls Stemness and Malignancy by suppressing CD133 Expression in Hepatocellular Carcinoma.Cancers · 2020Article
- A role for the p53 tumour suppressor in regulating the balance between homologous recombination and non-homologous end joining.Open biology · 2016Article
- Structure of human Cdc45 and implications for CMG helicase function.Nature communications · 2016Article
- Pharmacogenetics research on chemotherapy resistance in colorectal cancer over the last 20 years.World journal of gastroenterology · 2014Review
- A S-adenosylmethionine methyltransferase-like domain within the essential, Fe-S-containing yeast protein Dre2.The FEBS journal · 2012Article
- Srs2 overexpression reveals a helicase-independent role at replication forks that requires diverse cell functions.DNA repair · 2011Article
- Irinotecan pharmacogenomics.Pharmacogenomics · 2010Review
- Proteasome-dependent processing of topoisomerase I-DNA adducts into DNA double strand breaks at arrested replication forks.The Journal of biological chemistry · 2009Article
- A newly identified essential complex, Dre2-Tah18, controls mitochondria integrity and cell death after oxidative stress in yeast.PloS one · 2009Article
- TOR signaling is a determinant of cell survival in response to DNA damage.Molecular and cellular biology · 2007Article
- The role of DNA double-strand breaks in spontaneous homologous recombination in S. cerevisiae.PLoS genetics · 2006Article
- Distinct functional domains of Ubc9 dictate cell survival and resistance to genotoxic stress.Molecular and cellular biology · 2006Article
- Chromosomal fragmentation is the major consequence of the rdgB defect in Escherichia coli.Genetics · 2006Article
- Repair of topoisomerase I-mediated DNA damage.Progress in nucleic acid research and molecular biology · 2006Review
- Schizosaccharomyces pombe replication protein Cdc45/Sna41 requires Hsk1/Cdc7 and Rad4/Cut5 for chromatin binding.Chromosoma · 2004Article
- Mechanisms of resistance to topoisomerase I-targeting drugs.Oncogene · 2003Review
- Yeast recombination pathways triggered by topoisomerase II-mediated DNA breaks.Nucleic acids research · 2003Article
- Chromosome integrity in Saccharomyces cerevisiae: the interplay of DNA replication initiation factors, elongation factors, and origins.Genes & development · 2003Article
- Article
- Schizosaccharomyces pombe cells lacking the amino-terminal catalytic domains of DNA polymerase epsilon are viable but require the DNA damage checkpoint control.Molecular and cellular biology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The antitumor agent camptothecin targets DNA topoisomerase I by reversibly stabilizing a covalent enzyme-DNA intermediate. The subsequent collision of DNA replication forks with these drug-enzyme-DNA complexes produces the cytotoxic DNA lesions that signal cell cycle arrest and ultimately lead to cell death. Despite intense investigation, the character of the lesions produced and the repair processes that resolve the damage remain poorly defined. A yeast genetic screen was implemented to isolate conditional mutants with enhanced sensitivity to DNA topoisomerase I-mediated DNA damage. Cells exhibiting temperature-sensitive growth in the presence of the DNA topoisomerase I mutant, Top1T722Ap, were selected. Substitution of Ala for Thr722 increases the stability of the covalent Top1T722Ap-DNA intermediate, mimicking the cytotoxic action of camptothecin. Two mutants isolated, cdc45-10 and dpb11-10, exhibited specific defects in DNA replication and a synthetic lethal phenotype in the absence of DNA damaging agents. The accumulation of Okazaki fragments under nonpermissive conditions suggests a common function in promoting processive DNA replication through polymerase switching. These results provide a mechanistic basis for understanding the cellular processes involved in the resolution of DNA damage induced by camptothecin and DNA topoisomerase I.
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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.