ArticleOncogene2000
Proneness to UV-induced apoptosis in human fibroblasts defective in transcription coupled repair is associated with the lack of Mdm2 transactivation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 57 citations in OpenAlex.
- DNA damage and the balance between survival and death in cancer biology.Nature reviews. Cancer · 2016Review
- UVB-induced cell death signaling is associated with G1-S progression and transcription inhibition in primary human fibroblasts.PloS one · 2013Article
- CSA and CSB proteins interact with p53 and regulate its Mdm2-dependent ubiquitination.Cell cycle (Georgetown, Tex.) · 2011Article
- Involvement of global genome repair, transcription coupled repair, and chromatin remodeling in UV DNA damage response changes during development.PLoS genetics · 2010Article
- Cells from long-lived mutant mice exhibit enhanced repair of ultraviolet lesions.The journals of gerontology. Series A, Biological sciences and medical sciences · 2008Article
- DNA nucleotide excision repair-dependent signaling to checkpoint activation.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Enhanced repair of cyclobutane pyrimidine dimers and improved UV resistance in photolyase transgenic mice.The EMBO journal · 2002Article
- Article
- P53 plays a protective role against UV- and cisplatin-induced apoptosis in transcription-coupled repair proficient fibroblasts.Oncogene · 2001Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The apoptotic response and the level of expression of p53 and of three genes transcriptionally activated by p53 (Mdm2, p21 and bax) were investigated in UV-sensitive cells from patients with xeroderma pigmentosum (XP) or Cockayne syndrome (CS). These disorders are due to different genetic defects affecting transcription-coupled repair (TCR) and/or global genome repair (GGR), the nucleotide excision repair subpathways which remove UV-induced lesions from the transcribed strand of active genes or from the rest of the genome, respectively. After 20 J/m2 UV light, normal and GGR-defective XP-C fibroblasts showed rapid increase in p53, late induction of Mdm2 and no evidence of apoptosis even 96 h after irradiation. In contrast, in XP-A (defective in GGR and TCR), CS-A and CS-B (defective only in TCR) fibroblasts, the p53 increase was not followed by Mdm2 induction and the persistence of high levels of p53, due to the lack of its degradation by Mdm2, was associated with the appearance of apoptosis. Besides indicating that the persistence of DNA damage in the transcribed strand of active genes leads to apoptosis, these findings provide the first evidence that the lack of activation of Mdm2 plays a key role in the cascade of events leading to apoptosis. Oncogene (2000).
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