ArticleNature2016
Nucleotide excision repair is impaired by binding of transcription factors to DNA.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.
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Who cites it
200 citing papers in PubMed.
- The Impact of Environmental and Endogenous Damage on Somatic Mutation Load in Human Skin Fibroblasts.PLoS genetics · 2016Trial
- Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.Nucleic acids research · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Nature communications · 2026Article
- Mapping DNA glycosylase binding across lesion sequence contexts reveals extended sequence and structural recognition logic.Nature communications · 2026Article
- Sequence context and methylation interact to shape germline mutation rate variation at CpG sites.PLoS genetics · 2026Article
- DNA Mechanical Strain Steers Transcription Factor Recognition.Research square · 2026Article
- Sequence context and methylation interact to shape germline mutation rate variation at CpG sites.bioRxiv : the preprint server for biology · 2026Article
- Topographical archetypes of somatic mutagenesis in cancer.bioRxiv : the preprint server for biology · 2026Article
- Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacity.bioRxiv : the preprint server for biology · 2026Article
- Altered benzo[a]pyrene adduct formation in nucleosomes establishes distinct mutational patterns in lung cancer.The Journal of biological chemistry · 2026Article
- Melanin as a Redox Hub: Linking Energy Flow to Genome Stability and Immune Control.Antioxidants & redox signaling · 2026Review
- CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.iScience · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.bioRxiv : the preprint server for biology · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- Analysis of long-range contacts across cell types outlines a core sequence determinant of 3D genome organization.NAR genomics and bioinformatics · 2025Article
- Transcription start sites experience a high influx of heritable variants fueled by early development.Nature communications · 2025Article
- Dynamic genome-wide mapping reveals how chromatin context shapes OGG1-mediated repair and related mutagenesis in human cells.Nucleic acids research · 2025Article
- Topoisomerase IIb binding delineates localized mutational processes and driver mutations in cancer genomes.Nature communications · 2025Article
140 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic mutations are the driving force of cancer genome evolution. The rate of somatic mutations appears to be greatly variable across the genome due to variations in chromatin organization, DNA accessibility and replication timing. However, other variables that may influence the mutation rate locally are unknown, such as a role for DNA-binding proteins, for example. Here we demonstrate that the rate of somatic mutations in melanomas is highly increased at active transcription factor binding sites and nucleosome embedded DNA, compared to their flanking regions. Using recently available excision-repair sequencing (XR-seq) data, we show that the higher mutation rate at these sites is caused by a decrease of the levels of nucleotide excision repair (NER) activity. Our work demonstrates that DNA-bound proteins interfere with the NER machinery, which results in an increased rate of DNA mutations at the protein binding sites. This finding has important implications for our understanding of mutational and DNA repair processes and in the identification of cancer driver mutations.
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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.