ArticleNature cell biology2024
Transcription-coupled repair of DNA-protein cross-links depends on CSA and CSB.
Article in Nature cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed.
- Genomic Stress and DNA Repair During Macrophage Differentiation and Inflammatory Activation.International journal of molecular sciences · 2026Review
- Targeting the Mitochondrial Phenotype in Cockayne Syndrome Patient Cells: From Bioenergetic Fragility to Pharmacologic Rescue.bioRxiv : the preprint server for biology · 2026Article
- PAF1C restores transcription after DNA damage independently of promoting histone mark deposition.EMBO reports · 2026Article
- Integrator subunit INTS12 links ribotoxic stress to transcription-coupled nucleotide excision repair.Nature structural & molecular biology · 2026Article
- Living Cells Employ Ubiquitin-Proteasomal System and Nucleotide Excision Repair Pathways to Remove Reactive Oxygen Species-Induced DNA-Protein Crosslinks (ROS-DPCs).bioRxiv : the preprint server for biology · 2026Article
- DNA-Protein Cross-Link Formation and Cellular Toxicity by Chimeric Bis-Electrophiles.The Journal of organic chemistry · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Review
- Transcription-Coupled Repair Promotes the Retention of Mutations in Coding Regions During Replication Stress.International journal of molecular sciences · 2026Article
- Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II.Nature communications · 2026Article
- SPRTN preserves RNA polymerase I transcription under genotoxic drug stress in lung adenocarcinoma.Frontiers in oncology · 2026Article
- Cellular strategies for repairing trapped protein-DNA complexes.Frontiers in pharmacology · 2026Review
- Tissue-specific mutagenesis from endogenous guanine damage is suppressed by Polκ and DNA repair.Nature communications · 2025Article
- Molecular basis for CSB stimulation of the SNM1A DNA repair nuclease.Research square · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Examination of a Chimeric Bis-Electrophile for Selective DNA-Protein Cross-Linking and Mechlorethamine Reveals an Unknown Source of Nitrogen Mustard Cytotoxicity.Journal of the American Chemical Society · 2025Article
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- The molecular basis of human transcription-coupled DNA repair.Nature cell biology · 2025Review
- Wss1 and Ddi1 DNA-Protein crosslink repair proteases protect Saccharomyces cerevisiae and Candida albicans against oxidative stress.Scientific reports · 2025Article
- Allosteric activation of the SPRTN protease by ubiquitin maintains genome stability.Nature communications · 2025Article
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
Covalent DNA-protein cross-links (DPCs) are toxic DNA lesions that block replication and require repair by multiple pathways. Whether transcription blockage contributes to the toxicity of DPCs and how cells respond when RNA polymerases stall at DPCs is unknown. Here we find that DPC formation arrests transcription and induces ubiquitylation and degradation of RNA polymerase II. Using genetic screens and a method for the genome-wide mapping of DNA-protein adducts, DPC sequencing, we discover that Cockayne syndrome (CS) proteins CSB and CSA provide resistance to DPC-inducing agents by promoting DPC repair in actively transcribed genes. Consequently, CSB- or CSA-deficient cells fail to efficiently restart transcription after induction of DPCs. In contrast, nucleotide excision repair factors that act downstream of CSB and CSA at ultraviolet light-induced DNA lesions are dispensable. Our study describes a transcription-coupled DPC repair pathway and suggests that defects in this pathway may contribute to the unique neurological features of CS.
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Registered trials
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