ArticleNucleic acids research2016
A ubiquitylation site in Cockayne syndrome B required for repair of oxidative DNA damage, but not for transcription-coupled nucleotide excision repair.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Oxidative stress triggers RNAPII arrest through PARylation and DNA damage.Nature communications · 2026Article
- Transcription-Coupled Repair Promotes the Retention of Mutations in Coding Regions During Replication Stress.International journal of molecular sciences · 2026Article
- New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways.International journal of molecular sciences · 2024Review
- RNAPII response to transcription-blocking DNA lesions in mammalian cells.The FEBS journal · 2023Review
- Role of Cockayne Syndrome Group B Protein in Replication Stress: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- Article
- DNA glycosylase NEIL2 functions in multiple cellular processes.Progress in biophysics and molecular biology · 2021Review
- Review
- The Winged Helix Domain of CSB Regulates RNAPII Occupancy at Promoter Proximal Pause Sites.International journal of molecular sciences · 2021Article
- Cockayne syndrome group A and B proteins function in rRNA transcription through nucleolin regulation.Nucleic acids research · 2020Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- DNA Oxidation and Excision Repair Pathways.International journal of molecular sciences · 2019Review
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging.Nucleic acids research · 2019Article
- Structural basis of ubiquitin recognition by the winged-helix domain of Cockayne syndrome group B protein.Nucleic acids research · 2019Article
- Mechanistic insights into the regulation of transcription and transcription-coupled DNA repair by Cockayne syndrome protein B.Nucleic acids research · 2018Article
- Deoxyribonucleic Acid Damage and Repair: Capitalizing on Our Understanding of the Mechanisms of Maintaining Genomic Integrity for Therapeutic Purposes.International journal of molecular sciences · 2018Review
- Mechanistic and biological considerations of oxidatively damaged DNA for helicase-dependent pathways of nucleic acid metabolism.Free radical biology & medicine · 2017Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Cockayne syndrome B (CSB), best known for its role in transcription-coupled nucleotide excision repair (TC-NER), contains a ubiquitin-binding domain (UBD), but the functional connection between protein ubiquitylation and this UBD remains unclear. Here, we show that CSB is regulated via site-specific ubiquitylation. Mass spectrometry analysis of CSB identified lysine (K) 991 as a ubiquitylation site. Intriguingly, mutation of this residue (K991R) does not affect CSB's catalytic activity or protein stability, but greatly affects genome stability, even in the absence of induced DNA damage. Moreover, cells expressing CSB K991R are sensitive to oxidative DNA damage, but proficient for TC-NER. K991 becomes ubiquitylated upon oxidative DNA damage, and while CSB K991R is recruited normally to such damage, it fails to dissociate in a timely manner, suggesting a requirement for K991 ubiquitylation in CSB activation. Interestingly, deletion of CSB's UBD gives rise to oxidative damage sensitivity as well, while CSB ΔUBD and CSB K991R affects expression of overlapping groups of genes, further indicating a functional connection. Together, these results shed new light on the regulation of CSB, with K991R representing an important separation-of-function-mutation in this multi-functional protein.
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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.