ArticleMolecular and cellular biology2000
Repair of intermediate structures produced at DNA interstrand cross-links in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- Pooled it
- Deficiencies in the Fanconi anemia or homologous recombination pathway enhance the antitumor effects of the hypoxia-activated prodrug CP-506.Molecular therapy. Oncology · 2026Article
- NCAPH Stabilizes GEN1 in Chromatin to Resolve Ultra-Fine DNA Bridges and Maintain Chromosome Stability.Molecules and cells · 2022Article
- Visualization of uracils created by APOBEC3A using UdgX shows colocalization with RPA at stalled replication forks.Nucleic acids research · 2020Article
- Article
- XPF-ERCC1 protects liver, kidney and blood homeostasis outside the canonical excision repair pathways.PLoS genetics · 2020Article
- Limited Capacity or Involvement of Excision Repair, Double-Strand Breaks, or Translesion Synthesis for Psoralen Cross-Link Repair inGenetics · 2018Article
- Editor's Highlight: High-Throughput Functional Genomics Identifies Modulators of TCE Metabolite Genotoxicity and Candidate Susceptibility Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Replication and repair of a reduced 2΄-deoxyguanosine-abasic site interstrand cross-link in human cells.Nucleic acids research · 2017Article
- Cellular Repair of DNA-DNA Cross-Links Induced by 1,2,3,4-Diepoxybutane.International journal of molecular sciences · 2017Article
- A prosurvival DNA damage-induced cytoplasmic interferon response is mediated by end resection factors and is limited by Trex1.Genes & development · 2017Article
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016Review
- Mechanisms of interstrand DNA crosslink repair and human disorders.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2016Review
- Article
- Advances in understanding the complex mechanisms of DNA interstrand cross-link repair.Cold Spring Harbor perspectives in biology · 2013Review
- Pathways for repairing and tolerating the spectrum of oxidative DNA lesions.Cancer letters · 2012Review
- REV1 and DNA polymerase zeta in DNA interstrand crosslink repair.Environmental and molecular mutagenesis · 2012Review
- A prototypical Fanconi anemia pathway in lower eukaryotes?Cell cycle (Georgetown, Tex.) · 2012Article
- Fanconi-like crosslink repair in yeast.Genome integrity · 2012Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bifunctional alkylating agents and other drugs which produce DNA interstrand cross-links (ICLs) are among the most effective antitumor agents in clinical use. In contrast to agents which produce bulky adducts on only one strand of the DNA, the cellular mechanisms which act to eliminate DNA ICLs are still poorly understood, although nucleotide excision repair is known to play a crucial role in an early repair step. Using haploid Saccharomyces cerevisiae strains disrupted for genes central to the recombination, nonhomologous end-joining (NHEJ), and mutagenesis pathways, all these activities were found to be involved in the repair of nitrogen mustard (mechlorethamine)- and cisplatin-induced DNA ICLs, but the particular pathway employed is cell cycle dependent. Examination of whole chromosomes from treated cells using contour-clamped homogenous electric field electrophoresis revealed the intermediate in the repair of ICLs in dividing cells, which are mostly in S phase, to be double-strand breaks (DSBs). The origin of these breaks is not clear since they were still efficiently induced in nucleotide excision and base excision repair-deficient, mismatch repair-defective, rad27 and mre11 disruptant strains. In replicating cells, RAD52-dependent recombination and NHEJ both act to repair the DSBs. In contrast, few DSBs were observed in quiescent cells, and recombination therefore seems dispensable for repair. The activity of the Rev3 protein (DNA polymerase zeta) is apparently more important for the processing of intermediates in stationary-phase cells, since rev3 disruptants were more sensitive in this phase than in the exponential growth phase.
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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.