ReviewEnvironmental and molecular mutagenesis2010
Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle.
Review in Environmental and molecular mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 32 citations in OpenAlex.
- Oxidative Stress, Genetic Factors and Behavioral Responses to Chemical Exposure: Insights into Cancer Development in Zebrafish (Danio Rerio).Biochemical genetics · 2026Review
- RecA and RecB: probing complexes of DNA repair proteins with mitomycin C in liveJournal of the Royal Society, Interface · 2022Article
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Spectrin and its interacting partners in nuclear structure and function.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Autophagy Roles in the Modulation of DNA Repair Pathways.International journal of molecular sciences · 2017Review
- p97 Promotes a Conserved Mechanism of Helicase Unloading during DNA Cross-Link Repair.Molecular and cellular biology · 2016Article
- Nuclear alpha spectrin: Critical roles in DNA interstrand cross-link repair and genomic stability.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- DNA mismatch repair and the DNA damage response.DNA repair · 2016Review
- Mechanisms of interstrand DNA crosslink repair and human disorders.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2016Review
- Physical interaction between SLX4 (FANCP) and XPF (FANCQ) proteins and biological consequences of interaction-defective missense mutations.DNA repair · 2015Article
- DNA interstrand cross-link repair requires replication-fork convergence.Nature structural & molecular biology · 2015Article
- Meiotic interstrand DNA damage escapes paternal repair and causes chromosomal aberrations in the zygote by maternal misrepair.Scientific reports · 2015Article
- Mitomycin C reduces abundance of replication forks but not rates of fork progression in primary and transformed human cells.Oncoscience · 2014Article
- Fanconi-like crosslink repair in yeast.Genome integrity · 2012Article
- Rad5-dependent DNA repair functions of the Saccharomyces cerevisiae FANCM protein homolog Mph1.The Journal of biological chemistry · 2012Article
- Replication-coupled DNA interstrand cross-link repair in Xenopus egg extracts.Methods in molecular biology (Clifton, N.J.) · 2012Article
- Persistence and repair of bifunctional DNA adducts in tissues of laboratory animals exposed to 1,3-butadiene by inhalation.Chemical research in toxicology · 2011Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
DNA interstrand cross-linking (ICL) agents are widely used in anticancer chemotherapy regimens, yet our understanding of the DNA repair mechanisms by which these lesions are removed from the genome remains incomplete. This is at least in part due to the enormously complicated nature and variety of the biochemical pathways that operate on these complex lesions. In this review, we have focused specifically on the S-phase pathway of ICL repair in mammalian cells, which appears to be the major mechanism by which these lesions are removed in cycling cells. The various stages and components of this pathway are discussed, and a putative molecular model is presented. In addition, we propose an explanation as to how this pathway can lead to the observed high levels of sister chromatid exchanges known to be induced by ICLs.
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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.