ArticleOncogene2004
Nuclear accumulation of p53 following inhibition of transcription is not due to diminished levels of MDM2.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- Chromatin damage generated by DNA intercalators leads to degradation of RNA Polymerase II.Nucleic acids research · 2024Article
- Targeting cellular senescence to combat cancer and ageing.Molecular oncology · 2022Review
- CDK9 activity is critical for maintaining MDM4 overexpression in tumor cells.Cell death & disease · 2020Article
- DNA damage-induced ATM- and Rad-3-related (ATR) kinase activation in non-replicating cells is regulated by the XPB subunit of transcription factor IIH (TFIIH).The Journal of biological chemistry · 2017Article
- Nucleolar control of p53: a cellular Achilles' heel and a target for cancer therapy.Cellular and molecular life sciences : CMLS · 2014Review
- Article
- The nucleolus directly regulates p53 export and degradation.The Journal of cell biology · 2011Article
- Mechanistic insight into DNA damage and repair in ischemic stroke: exploiting the base excision repair pathway as a model of neuroprotection.Antioxidants & redox signaling · 2011Review
- The ubiquitin-proteasome system regulates p53-mediated transcription at p21waf1 promoter.Oncogene · 2007Article
- The p53-targeting human phosphatase hCdc14A interacts with the Cdk1/cyclin B complex and is differentially expressed in human cancers.Molecular cancer · 2006Article
- Recruitment of DNA damage checkpoint proteins to damage in transcribed and nontranscribed sequences.Molecular and cellular biology · 2006Article
- Human hHpr1/p84/Thoc1 regulates transcriptional elongation and physically links RNA polymerase II and RNA processing factors.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A common mechanism by which the tumor suppressor p53 accumulates in the nucleus following cellular stress is through the attenuation of its interaction with MDM2, a protein involved in the nuclear export and degradation of p53. This is accomplished by induced modifications of p53, MDM2 or both. We have previously found that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) induces the nuclear accumulation of p53 without concomitant phosphorylation of the ser15 site of p53, which is thought to be a modification important for the attenuation of p53-MDM2 interaction. It has been proposed that the mechanism by which p53 accumulates following blockage of transcription involves the downregulation of MDM2 expression. In this study, we tested this hypothesis and found that after DRB treatment, p53 accumulated despite the fact that MDM2 levels remained high in human cells. Furthermore, over expression of MDM2 did not prevent the accumulation of p53 following DRB treatment. In, addition, p53 accumulating in the nucleus after DRB treatment was able to interact with MDM2 and was ubiquitylated. These findings suggest that blockage of transcription induce the nuclear accumulation of p53 without breaking the p53-MDM2 regulation loop.
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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.