ArticleOncogene2002
A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 132 citations in OpenAlex.
- Review
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Obesity and cancer: A mechanistic overview of metabolic changes in obesity that impact genetic instability.Molecular carcinogenesis · 2019Review
- Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019Article
- The transcription-coupled DNA repair-initiating protein CSB promotes XRCC1 recruitment to oxidative DNA damage.Nucleic acids research · 2018Article
- Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome.Journal of molecular biology · 2016Article
- Dysregulation of gene expression as a cause of Cockayne syndrome neurological disease.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- DNA repair diseases: What do they tell us about cancer and aging?Genetics and molecular biology · 2014Review
- Modulation of base excision repair of 8-oxoguanine by the nucleotide sequence.Nucleic acids research · 2013Article
- Mammalian transcription-coupled excision repair.Cold Spring Harbor perspectives in biology · 2013Review
- Nucleotide excision repair-initiating proteins bind to oxidative DNA lesions in vivo.The Journal of cell biology · 2012Article
- Mfd is required for rapid recovery of transcription following UV-induced DNA damage but not oxidative DNA damage in Escherichia coli.Journal of bacteriology · 2012Article
- Downregulation of Cockayne syndrome B protein reduces human 8-oxoguanine DNA glycosylase-1 expression and repair of UV radiation-induced 8-oxo-7,8-dihydro-2'-deoxyguanine.Cancer science · 2011Article
- 8-Oxo-7,8-dihydroguanine in DNA does not constitute a barrier to transcription, but is converted into transcription-blocking damage by OGG1.Nucleic acids research · 2011Article
- Early host cell reactivation of an oxidatively damaged adenovirus-encoded reporter gene requires the Cockayne syndrome proteins CSA and CSB.Mutagenesis · 2011Article
- Cockayne syndrome B protects against methamphetamine-enhanced oxidative DNA damage in murine fetal brain and postnatal neurodevelopmental deficits.Antioxidants & redox signaling · 2011Article
- Mitochondrial base excision repair assays.Methods (San Diego, Calif.) · 2010Review
- Cockayne syndrome group B protein promotes mitochondrial DNA stability by supporting the DNA repair association with the mitochondrial membrane.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Cockayne syndrome group B protein stimulates repair of formamidopyrimidines by NEIL1 DNA glycosylase.The Journal of biological chemistry · 2009Article
- Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (steady-state) levels of oxidative DNA modifications in cells from csb(-/-) mice were not different from those in wild-type mice and did not increase with age. The analysis of the repair rates of additional oxidative DNA base modifications induced by photosensitization in immortalized embryonic fibroblasts was in accordance with these findings: compared to wild-type cells, the global repair was only slightly affected in csb(-/-) cells, more compromised in ogg1(-/-) cells, but virtually absent in csb(-/-)/ogg1(-/-) cells. An inhibition of transcription by alpha-amanitin did not block the Csb-dependent repair in ogg1(-/-) fibroblasts. The influence of Csb on the global repair of 8-oxoG was not detectable in assays with total protein extracts and in a shuttle vector system. The data indicate a role for Csb in the removal of 8-oxoG from the overall genome that is independent of both Ogg1-mediated base excision repair and regular transcription.
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