ArticleNucleic acids research2003
Functional consequences of mutations in the conserved SF2 motifs and post-translational phosphorylation of the CSB protein.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- PARP1 and PARylation facilitate transcription-coupled DNA repair by stabilizing the CSB-RNAPII complex.Nucleic acids research · 2025Article
- Phosphorylation of the Human DNA Glycosylase NEIL2 Is Affected by Oxidative Stress and Modulates Its Activity.Antioxidants (Basel, Switzerland) · 2023Article
- Mechanism of Rad26-assisted rescue of stalled RNA polymerase II in transcription-coupled repair.Nature communications · 2021Article
- Whole Exome Sequencing Identifies a Novel Homozygous Missense Mutation in the CSB Protein-EncodingLife (Basel, Switzerland) · 2021Article
- Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- DNA-mediated coupling of ATPase, translocase and nuclease activities of a Type ISP restriction-modification enzyme.Nucleic acids research · 2020Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Multiomic Analysis of the UV-Induced DNA Damage Response.Cell reports · 2016Article
- CSB interacts with SNM1A and promotes DNA interstrand crosslink processing.Nucleic acids research · 2015Article
- Cockayne Syndrome group B protein stimulates NEIL2 DNA glycosylase activity.Mechanisms of ageing and development · 2014Article
- Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Genetic variability in DNA repair proteins in age-related macular degeneration.International journal of molecular sciences · 2012Review
- Human Cockayne syndrome B protein reciprocally communicates with mitochondrial proteins and promotes transcriptional elongation.Nucleic acids research · 2012Article
- Expressing genes do not forget their LINEs: transposable elements and gene expression.Frontiers in bioscience (Landmark edition) · 2012Review
- Molecular cloning and gene expression analysis of Ercc6l in Sika deer (Cervus nippon hortulorum).PloS one · 2011Article
- Nucleic acid binding activity of human Cockayne syndrome B protein and identification of Ca(2+) as a novel metal cofactor.Journal of molecular biology · 2009Article
- Cockayne syndrome group B protein is engaged in processing of DNA adducts of lipid peroxidation product trans-4-hydroxy-2-nonenal.Mutation research · 2009Article
- Cockayne syndrome group B protein stimulates repair of formamidopyrimidines by NEIL1 DNA glycosylase.The Journal of biological chemistry · 2009Article
- An abundant evolutionarily conserved CSB-PiggyBac fusion protein expressed in Cockayne syndrome.PLoS genetics · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The rare inherited human genetic disorder Cockayne syndrome (CS) is characterized by developmental abnormalities, UV sensitivity and premature aging. The cellular and molecular phenotypes of CS include increased sensitivity to UV-induced and oxidative DNA lesions. Two genes are involved: CSA and CSB. The CS group B (CSB) protein has roles in transcription, transcription-coupled repair, and base excision repair. It is a DNA stimulated ATPase and remodels chromatin in vitro. Here, we have analyzed wild-type (wt) and motif II, V and VI mutant CSB proteins. We find that the mutant proteins display different degrees of ATPase activity deficiency, and in contrast to the in vivo complementation studies, the motif II mutant is more defective than motif V and VI CSB mutants. Furthermore, CSB wt ATPase activity was studied with different biologically important DNA cofactors: DNA with different secondary structures and damaged DNA. The results indicate that the state of DNA secondary structure affects the level of CSB ATPase activity. We find that the CSB protein is phosphorylated in untreated cells and that UV irradiation leads to its dephosphorylation. Importantly, dephosphorylation of the protein in vitro results in increased ATPase activity of the protein, suggesting that the activity of the CSB protein is subject to phosphorylation control in vivo. These observations may have significant implications for the function of CSB in vivo.
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Registered trials
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