ArticleCell reports2017
Sensing and Processing of DNA Interstrand Crosslinks by the Mismatch Repair Pathway.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed.
- Structural insights into predicted protein-protein interactions and protein complexes in the human proteome.Scientific reports · 2026Article
- Mismatch repair deficiency reshapes glioblastoma through immune suppression rather than hypermutation.The Journal of clinical investigation · 2026Article
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- The Fanconi anemia pathway repairs colibactin-induced DNA interstrand cross-links.Nature communications · 2025Article
- Synthesis of Oligonucleotides Containing a Dna Distorting Interstrand Crosslink Produced by Mitomycins.Chembiochem : a European journal of chemical biology · 2025Article
- Embryonic Stem Cell-Specific Responses to DNA Replication Stress.bioRxiv : the preprint server for biology · 2025Article
- Dietary fibre counters the oncogenic potential of colibactin-producing Escherichia coli in colorectal cancer.Nature microbiology · 2025Article
- The novel DNA cross-linking agent KL-50 is active against patient-derived models of new and recurrent post-temozolomide mismatch repair-deficient glioblastoma.Neuro-oncology · 2025Article
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.PNAS nexus · 2024Article
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- A critical review of ethanol effects on neuronal firing: A metabolic perspective.Alcohol, clinical & experimental research · 2024Review
- Detection of oxaliplatin- and cisplatin-DNA lesions requires different global genome repair mechanisms that affect their clinical efficacy.NAR cancer · 2023Article
- Combining targeted DNA repair inhibition and immune-oncology approaches for enhanced tumor control.Molecular cell · 2023Review
- PD-1/PD-L1 and DNA Damage Response in Cancer.Cells · 2023Review
- Chronic alcohol metabolism results in DNA repair infidelity and cell cycle-induced senescence in neurons.Aging cell · 2023Article
- A CRISPR-Cas9 screen identifies EXO1 as a formaldehyde resistance gene.Nature communications · 2023Article
- Comparative analysis of chlorambucil-induced DNA lesion formation and repair in a spectrum of different human cell systems.Toxicology reports · 2023Article
- Cytotoxicity, crosslinking and biological activity of three mitomycins.Bioorganic chemistry · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
DNA interstrand crosslinks (ICLs) that are repaired in non-dividing cells must be recognized independently of replication-associated DNA unwinding. Using cell-free extracts from Xenopus eggs that support neither replication nor transcription, we establish that ICLs are recognized and processed by the mismatch repair (MMR) machinery. We find that ICL repair requires MutSα (MSH2-MSH6) and the mismatch recognition FXE motif in MSH6, strongly suggesting that MutSα functions as an ICL sensor. MutSα recruits MutLα and EXO1 to ICL lesions, and the catalytic activity of both these nucleases is essential for ICL repair. As anticipated for a DNA unwinding-independent recognition process, we demonstrate that least distorting ICLs fail to be recognized and repaired by the MMR machinery. This establishes that ICL structure is a critical determinant of repair efficiency outside of DNA replication.
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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.