2003
DOI: 10.1038/sj.onc.1206187
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The transcriptional response after oxidative stress is defective in Cockayne syndrome group B cells

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Cited by 63 publications
(49 citation statements)
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“…It has been hypothesized that CSB would induce transcription of genes encoding DNA glycosylases such as OGG1 (Dianov et al, 1999;Tuo et al, 2002). Suggestion of a defect in the transcriptional response of CS-B cells after H 2 O 2 treatment has been provided (Kyng et al, 2003) and a recent study demonstrates that CSB is involved in the regulation of the transcriptional program after UV damage (Proietti-De-Santis et al, 2006). It would be interesting to analyse further the role of CS proteins in transcription regulation after oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…It has been hypothesized that CSB would induce transcription of genes encoding DNA glycosylases such as OGG1 (Dianov et al, 1999;Tuo et al, 2002). Suggestion of a defect in the transcriptional response of CS-B cells after H 2 O 2 treatment has been provided (Kyng et al, 2003) and a recent study demonstrates that CSB is involved in the regulation of the transcriptional program after UV damage (Proietti-De-Santis et al, 2006). It would be interesting to analyse further the role of CS proteins in transcription regulation after oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…CSB stimulates transcription by stimulating elongation of actively transcribing RNA polymerase bound to DNA and nascent RNA (Selby and Sancar, 1997a;Tantin et al, 1997;. Furthermore, using array analysis, Kyng et al (Kyng et al, 2003) demonstrated that the transcriptional response after oxidative stress is defective in CSB cells. Some of the major defects were found to be in the transcription of genes involved in DNA repair, signal transduction and ribosomal functions.…”
Section: The Role Of Csb In Various Cellular Processesmentioning
confidence: 99%
“…There has been considerable discussion about whether the complex clinical phenotype of CS is due to a primary defect in DNA repair or transcription. Much data including array analysis by Kyng et al (Kyng et al, 2003) would suggest that a major defect in this disease lies in the transcriptional response to oxidative stress. This is compatible with the substantial amounts of data suggesting that progeria in CS is linked to accumulated endogenous DNA damage (Andressoo et al, 2006).…”
Section: The Role Of Csb In Dna Repair -And Consequences For the Aginmentioning
confidence: 99%
“…Mutations in XPB and XPD affect specific expression of nuclear hormone receptors that are important in development including the retinoic acid receptors RARalpha, ERalpha, and AR (Keriel et al, 2002), which may account for part of the wasting phenotype of XP/CS patients. Microarray analysis of CSB cells has detected multiple changes in gene expression associated with the response to oxidative stress, signal transduction, ribosomal synthesis and uracil-Dglycosylase (Kyng et al, 2003). We have also found several specific gene expression markers of CSB in a microarray analysis that compared parent child pairs from CS-B families (Hefner et al, 2006).…”
Section: Csa (Ercc8)mentioning
confidence: 75%