ReviewNature reviews. Molecular cell biology2026
Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.
Review in Nature reviews. Molecular cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Transcription remodeling and stalling by cisplatin-induced interstrand crosslinks.Nature chemical biology · 2026Article
- The dark side of DNA repair: when genome maintenance runs out of fuel.Cell research · 2026Article
- Silver-based N-heterocyclic carbene (NHC) complexes as emerging strategies against antimicrobial resistance.Archives of microbiology · 2026Review
- Article
- Polymerase face-off: emerging concepts in transcription-replication coordination.EMBO reports · 2026Review
- RNA damage signaling primes transcription-coupled repair.Nature structural & molecular biology · 2026Article
- PAF1C restores transcription after DNA damage independently of promoting histone mark deposition.EMBO reports · 2026Article
- Structural basis of transcription-coupled RNA damage by incorporation of oxidized ribonucleotides.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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.
Funding
Abstract
RNA polymerase II (Pol II)-mediated gene transcription is frequently disrupted by DNA damage from various sources. Transcription-blocking DNA lesions hinder the progression of elongating Pol II, leading to transcription stress that, if unresolved, causes cellular dysfunction, neurodegeneration and ageing. In this Review, we discuss how different types of lesion are recognized by obstructing Pol II and removed by the intricate transcription-coupled nucleotide excision repair (TC-NER) pathway, emphasizing recent structural findings that reveal key aspects of the TC-NER mechanism. We also discuss the mechanisms proposed for processing lesion-stalled Pol II, which is crucial to facilitate TC-NER, and focus on how Pol II ubiquitylation orchestrates repair-complex assembly and Pol II degradation. In addition, we discuss the alternative mechanism of transcription-coupled DNA-protein crosslink repair, which was recently identified to be important for resolving DNA-protein crosslinks in active genes. Finally, we describe how these insights elucidate the different pathological causes of hereditary TC-NER deficiencies, namely of the mild cutaneous ultraviolet-sensitive syndrome and the severe progeroid Cockayne syndrome.
Identifiers
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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.