ArticleJournal of molecular biology2016
Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome.
Article in Journal of molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Meta-analysis of DNA double-strand break response kinetics.Nucleic acids research · 2017Pooled it
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- Perspectives in the investigation of Cockayne syndrome group B neurological disease: the utility of patient-derived brain organoid models.Journal of Zhejiang University. Science. B · 2024Review
- Article
- A CRISPR-Cas9 screen identifies EXO1 as a formaldehyde resistance gene.Nature communications · 2023Article
- LEO1 is a partner for Cockayne syndrome protein B (CSB) in response to transcription-blocking DNA damage.Nucleic acids research · 2021Article
- Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Cockayne syndrome group A and B proteins function in rRNA transcription through nucleolin regulation.Nucleic acids research · 2020Article
- Review
- Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism.Annual review of biochemistry · 2019Review
- Genomic instability and DNA replication defects in progeroid syndromes.Nucleus (Austin, Tex.) · 2018Review
- Regulation of the Intranuclear Distribution of the Cockayne Syndrome Proteins.Scientific reports · 2018Article
- Differential RPA-1 and RAD-51 recruitment in vivo throughout the C. elegans germline, as revealed by laser microirradiation.Nucleic acids research · 2018Article
- ATM and CDK2 control chromatin remodeler CSB to inhibit RIF1 in DSB repair pathway choice.Nature communications · 2017Article
- Are parents of children with Cockayne syndrome manifesting features of the disorder?: Case reports.Medicine · 2017Article
- Mechanistic and biological considerations of oxidatively damaged DNA for helicase-dependent pathways of nucleic acid metabolism.Free radical biology & medicine · 2017Review
- Cockayne syndrome B protein regulates recruitment of the Elongin A ubiquitin ligase to sites of DNA damage.The Journal of biological chemistry · 2017Article
- A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine.Nucleic acids research · 2017Article
- Transcription-coupled repair: an update.Archives of toxicology · 2016Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cockayne syndrome (CS) is a premature aging disorder characterized by developmental defects, multisystem progressive degeneration and sensitivity to ultraviolet light. CS is divided into two primary complementation groups, A and B, with the CSA and CSB proteins presumably functioning in DNA repair and transcription. Using laser microirradiation and confocal microscopy, we characterized the nature and regulation of the CS protein response to oxidative DNA damage, double-strand breaks (DSBs), angelicin monoadducts and trioxsalen interstrand crosslinks (ICLs). Our data indicate that CSB recruitment is influenced by the type of DNA damage and is most rapid and robust as follows: ICLs>DSBs>monoadducts>oxidative lesions. Transcription inhibition reduced accumulation of CSB at sites of monoadducts and ICLs, but it did not affect recruitment to (although slightly affected retention at) oxidative damage. Inhibition of histone deacetylation altered the dynamics of CSB assembly, suggesting a role for chromatin status in the response to DNA damage, whereas the proteasome inhibitor MG132 had no effect. The C-terminus of CSB and, in particular, its ubiquitin-binding domain were critical to recruitment, while the N-terminus and a functional ATPase domain played a minor role at best in facilitating protein accumulation. Although the absence of CSA had no effect on CSB recruitment, CSA itself localized at sites of ICLs, DSBs and monoadducts but not at oxidative lesions. Our results reveal molecular components of the CS protein response and point to a major involvement of complex lesions in the pathology of CS.
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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.