ArticleMolecular and cellular biology1997
Recognition and repair of compound DNA lesions (base damage and mismatch) by human mismatch repair and excision repair systems.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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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.
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Who cites it
64 citing papers in PubMed, 198 citations in OpenAlex.
- RNA/DNA-binding protein TDP43 regulates DNA mismatch repair genes with implications for genome stability.Nucleic acids research · 2025Article
- The negligible mutagenic effects of norfloxacin on the genome of the fission yeastMicrobiology spectrum · 2025Article
- RNA/DNA Binding Protein TDP43 Regulates DNA Mismatch Repair Genes with Implications for Genome Stability.bioRxiv : the preprint server for biology · 2025Article
- The interplay of 3D genome organization with UV-induced DNA damage and repair.The Journal of biological chemistry · 2023Article
- Reactive Acrylamide-Modified DNA Traps for Accurate Cross-Linking with Cysteine Residues in DNA-Protein Complexes Using Mismatch Repair Protein MutS as a Model.Molecules (Basel, Switzerland) · 2022Article
- CSB-independent, XPC-dependent transcription-coupled repair inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- H3K36me3-mediated mismatch repair preferentially protects actively transcribed genes from mutation.The Journal of biological chemistry · 2018Article
- Nucleotide Excision Repair Lesion-Recognition Protein Rad4 Captures a Pre-Flipped Partner Base in a Benzo[a]pyrene-Derived DNA Lesion: How Structure Impacts the Binding Pathway.Chemical research in toxicology · 2017Article
- Mismatch repair proteins recruited to ultraviolet light-damaged sites lead to degradation of licensing factor Cdt1 in the G1 phase.Cell cycle (Georgetown, Tex.) · 2017Article
- Recognition of Damaged DNA for Nucleotide Excision Repair: A Correlated Motion Mechanism with a Mismatched cis-syn Thymine Dimer Lesion.Biochemistry · 2015Article
- A novel DNA damage response mediated by DNA mismatch repair in Caenorhabditis elegans: induction of programmed autophagic cell death in non-dividing cells.Genes & cancer · 2015Article
- Genome-wide analysis of human global and transcription-coupled excision repair of UV damage at single-nucleotide resolution.Genes & development · 2015Article
- Oxidative stress in aging human skin.Biomolecules · 2015Review
- FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.Cancer research · 2014Article
- Is thymidine glycol containing DNA a substrate of E. coli DNA mismatch repair system?PloS one · 2014Article
- Ligand modulation of a dinuclear platinum compound leads to mechanistic differences in cell cycle progression and arrest.Biochemical pharmacology · 2013Article
- Removal of misincorporated ribonucleotides from prokaryotic genomes: an unexpected role for nucleotide excision repair.PLoS genetics · 2013Article
- Nucleotide excision repair in human cells: fate of the excised oligonucleotide carrying DNA damage in vivo.The Journal of biological chemistry · 2013Article
- New synthetic substrates of mammalian nucleotide excision repair system.Nucleic acids research · 2013Article
4 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
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Nucleotide excision repair and the long-patch mismatch repair systems correct abnormal DNA structures arising from DNA damage and replication errors, respectively. DNA synthesis past a damaged base (translesion replication) often causes misincorporation at the lesion site. In addition, mismatches are hot spots for DNA damage because of increased susceptibility of unpaired bases to chemical modification. We call such a DNA lesion, that is, a base damage superimposed on a mismatch, a compound lesion. To learn about the processing of compound lesions by human cells, synthetic compound lesions containing UV photoproducts or cisplatin 1,2-d(GpG) intrastrand cross-link and mismatch were tested for binding to the human mismatch recognition complex hMutS alpha and for excision by the human excision nuclease. No functional overlap between excision repair and mismatch repair was observed. The presence of a thymine dimer or a cisplatin diadduct in the context of a G-T mismatch reduced the affinity of hMutS alpha for the mismatch. In contrast, the damaged bases in these compound lesions were excised three- to fourfold faster than simple lesions by the human excision nuclease, regardless of the presence of hMutS alpha in the reaction. These results provide a new perspective on how excision repair, a cellular defense system for maintaining genomic integrity, can fix mutations under certain circumstances.
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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.