ArticleNucleic acids research2017
Common TFIIH recruitment mechanism in global genome and transcription-coupled repair subpathways.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 122 citations in OpenAlex.
- UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair.The Journal of biological chemistry · 2026Article
- Genome-wide association analysis of treatment response to onabotulinumtoxinA in Han Chinese patients with chronic migraine: a pilot study.BMC neurology · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- The interaction of XPG with TFIIH through p62 and XPD is required for the completion of nucleotide excision repair.Nucleic acids research · 2026Article
- Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II.Nature communications · 2026Article
- Dynamic networks of intrinsically disordered regions in nuclear proteins.Biophysics and physicobiology · 2026Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- A deep learning method for predicting interactions for intrinsically disordered regions of proteins.bioRxiv : the preprint server for biology · 2025Article
- The molecular basis of human transcription-coupled DNA repair.Nature cell biology · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Molecular model of TFIIH recruitment to the transcription-coupled repair machinery.Nature communications · 2025Article
- Article
- STK19 facilitates the clearance of lesion-stalled RNAPII during transcription-coupled DNA repair.Cell · 2024Article
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
- Differential processing of RNA polymerase II at DNA damage correlates with transcription-coupled repair syndrome severity.Nucleic acids research · 2024Article
- Review
- Coordination of transcription-coupled repair and repair-independent release of lesion-stalled RNA polymerase II.Nature communications · 2024Article
- Elf1 promotes transcription-coupled repair in yeast by using its C-terminal domain to bind TFIIH.Nature communications · 2024Article
- STK19 positions TFIIH for cell-free transcription-coupled DNA repair.bioRxiv : the preprint server for biology · 2024Article
- The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide excision repair is initiated by two different damage recognition subpathways, global genome repair (GGR) and transcription-coupled repair (TCR). In GGR, XPC detects DNA lesions and recruits TFIIH via interaction with the pleckstrin homology (PH) domain of TFIIH subunit p62. In TCR, an elongating form of RNA Polymerase II detects a lesion on the transcribed strand and recruits TFIIH by an unknown mechanism. Here, we found that the TCR initiation factor UVSSA forms a stable complex with the PH domain of p62 via a short acidic string in the central region of UVSSA, and determined the complex structure by NMR. The acidic string of UVSSA binds strongly to the basic groove of the PH domain by inserting Phe408 and Val411 into two pockets, highly resembling the interaction mechanism of XPC with p62. Mutational binding analysis validated the structure and identified residues crucial for binding. TCR activity was markedly diminished in UVSSA-deficient cells expressing UVSSA mutated at Phe408 or Val411. Thus, a common TFIIH recruitment mechanism is shared by UVSSA in TCR and XPC in GGR.
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.