ArticleProceedings of the National Academy of Sciences of the United States of America2023
UV irradiation remodels the specificity landscape of transcription factors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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.
- 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
- Article
- CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.iScience · 2026Article
- 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
- Life Factors and Melanoma: From the Macroscopic State to the Molecular Mechanism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Article
- The ethylene response factor ERF1A regulates UV-C-induced delayed ripening in peach fruit.Plant physiology · 2025Article
- Multi-Omics and Molecular Docking Studies on Caffeine for Its Skin Rejuvenating Potentials.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Light-Driven Enzyme Catalysis: Ultrafast Mechanisms and Biochemical Implications.Biochemistry · 2025Review
- Genome-wide maps of UV damage repair and mutation suppression by CPD photolyase.Nucleic acids research · 2025Article
- UVREK: Development and Analysis of an Expression Profile Knowledgebase of Biomolecules Induced by Ultraviolet Radiation Exposure.ACS omega · 2025Article
- High UV damage and low repair, but not cytosine deamination, stimulate mutation hotspots at ETS binding sites in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcription and DNA repair collide after UV exposure.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- UV irradiation remodels the specificity landscape of transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Deciphering the dynamic code: DNA recognition by transcription factors in the ever-changing genome.TranscriptionReview
- Illuminating genome repair by photolyase.Photochemistry and photobiologyArticle
Corrections and comments
- Commented on by
Authors and funding
13 authors.
Funding
Abstract
Somatic mutations are highly enriched at transcription factor (TF) binding sites, with the strongest trend being observed for ultraviolet light (UV)-induced mutations in melanomas. One of the main mechanisms proposed for this hypermutation pattern is the inefficient repair of UV lesions within TF-binding sites, caused by competition between TFs bound to these lesions and the DNA repair proteins that must recognize the lesions to initiate repair. However, TF binding to UV-irradiated DNA is poorly characterized, and it is unclear whether TFs maintain specificity for their DNA sites after UV exposure. We developed UV-Bind, a high-throughput approach to investigate the impact of UV irradiation on protein-DNA binding specificity. We applied UV-Bind to ten TFs from eight structural families, and found that UV lesions significantly altered the DNA-binding preferences of all the TFs tested. The main effect was a decrease in binding specificity, but the precise effects and their magnitude differ across factors. Importantly, we found that despite the overall reduction in DNA-binding specificity in the presence of UV lesions, TFs can still compete with repair proteins for lesion recognition, in a manner consistent with their specificity for UV-irradiated DNA. In addition, for a subset of TFs, we identified a surprising but reproducible effect at certain nonconsensus DNA sequences, where UV irradiation leads to a high increase in the level of TF binding. These changes in DNA-binding specificity after UV irradiation, at both consensus and nonconsensus sites, have important implications for the regulatory and mutagenic roles of TFs in the cell.
Indexed as
Identifiers
What OpenQuestion holds
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.