ArticleNature genetics2012
UV-sensitive syndrome protein UVSSA recruits USP7 to regulate transcription-coupled repair.
Article in Nature genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 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
158 citing papers in PubMed, 266 citations in OpenAlex.
- Topology Resetting During Transcription-Coupled Nucleotide Excision Repair.International journal of molecular sciences · 2026Review
- Proteome-wide Ubiquitinome Profiling Reveals Substrate-specific Dynamics Within the USP7 Network.Molecular & cellular proteomics : MCP · 2026Article
- Ubiquitin's code: UPS orchestrating DNA repair and genomic stability under genotoxic stress.Molecular and cellular biochemistry · 2026Review
- The Plasma Glycoprotein Milieu in the Hemato-Oncological Patient Inhibits Platelet Function.Biomolecules · 2026Article
- Transcription-coupled nucleotide excision repair protects against genomic instability and cell death induced by the liver toxin methyleugenol.Cell death & disease · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Genome-wide single-cell perturbation screens with VIPerturb-seq.bioRxiv : the preprint server for biology · 2026Article
- DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.Scientific reports · 2026Article
- STAG2-truncating variants reveal a mosaic STAG2 inactivation pattern and compensatory mechanisms involving cohesin complex remodeling.iScience · 2025Article
- Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025Review
- PARP1 and PARylation facilitate transcription-coupled DNA repair by stabilizing the CSB-RNAPII complex.Nucleic acids research · 2025Article
- 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
- KIF2A stabilizes intercellular bridge microtubules to maintain mouse embryonic stem cell cytokinesis.The Journal of cell biology · 2025Article
- Transcription-Coupled Repair and R-Loop Crosstalk in Genome Stability.International journal of molecular sciences · 2025Review
- Molecular model of TFIIH recruitment to the transcription-coupled repair machinery.Nature communications · 2025Article
- Article
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
98 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Transcription-coupled nucleotide-excision repair (TC-NER) is a subpathway of NER that efficiently removes the highly toxic RNA polymerase II blocking lesions in DNA. Defective TC-NER gives rise to the human disorders Cockayne syndrome and UV-sensitive syndrome (UV(S)S). NER initiating factors are known to be regulated by ubiquitination. Using a SILAC-based proteomic approach, we identified UVSSA (formerly known as KIAA1530) as part of a UV-induced ubiquitinated protein complex. Knockdown of UVSSA resulted in TC-NER deficiency. UVSSA was found to be the causative gene for UV(S)S, an unresolved NER deficiency disorder. The UVSSA protein interacts with elongating RNA polymerase II, localizes specifically to UV-induced lesions, resides in chromatin-associated TC-NER complexes and is implicated in stabilizing the TC-NER master organizing protein ERCC6 (also known as CSB) by delivering the deubiquitinating enzyme USP7 to TC-NER complexes. Together, these findings indicate that UVSSA-USP7–mediated stabilization of ERCC6 represents a critical regulatory mechanism of TC-NER in restoring gene expression.
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.