ArticleOncogene2006
p53 tumor suppressor protein regulates the levels of huntingtin gene expression.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
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- Exploring the role of high-mobility group box 1 (HMGB1) protein in the pathogenesis of Huntington's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- High-mobility group box 1 links sensing of reactive oxygen species by huntingtin to its nuclear entry.The Journal of biological chemistry · 2019Article
- A patient-derived cellular model for Huntington's disease reveals phenotypes at clinically relevant CAG lengths.Molecular biology of the cell · 2018Article
- Attenuation of Glutamate-Induced Excitotoxicity by Withanolide-A in Neuron-Like Cells: Role for PI3K/Akt/MAPK Signaling Pathway.Molecular neurobiology · 2018Article
- Transcriptional Dysregulation and Post-translational Modifications in Polyglutamine Diseases: From Pathogenesis to Potential Therapeutic Strategies.Frontiers in molecular neuroscience · 2018Review
- Transcriptional Regulation of the Huntingtin Gene.Journal of Huntington's disease · 2018Review
- A Mitochondria-Associated Oxidative Stress Perspective on Huntington's Disease.Frontiers in molecular neuroscience · 2018Review
- Possible Role of the Polyglutamine Elongation in Evolution of Amyloid-Related Evolvability.Journal of Huntington's disease · 2018Article
- Reduced cell size, chromosomal aberration and altered proliferation rates are characteristics and confounding factors in the STHdh cell model of Huntington disease.Scientific reports · 2017Article
- Huntington's Disease and Mitochondria.Neurotoxicity research · 2017Review
- P53 Dysfunction in Neurodegenerative Diseases - The Cause or Effect of Pathological Changes?Aging and disease · 2017Review
- Is Huntingtin Dispensable in the Adult Brain?Journal of Huntington's disease · 2017Review
- Huntingtin N17 domain is a reactive oxygen species sensor regulating huntingtin phosphorylation and localization.Human molecular genetics · 2016Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 protein is a transcription factor that integrates various cellular stress signals. The accumulation of the mutant huntingtin protein with an expanded polyglutamine tract plays a central role in the pathology of human Huntington's disease. We found that the huntingtin gene contains multiple putative p53-responsive elements and p53 binds to these elements both in vivo and in vitro. p53 activation in cultured human cells, either by a temperature-sensitive mutant p53 protein or by gamma-irradiation (gamma-irradiation), increases huntingtin mRNA and protein expression. Similarly, murine huntingtin also contains multiple putative p53-responsive elements and its expression is induced by p53 activation in cultured cells. Moreover, gamma-irradiation, which activates p53, increases huntingtin gene expression in the striatum and cortex of mouse brain, the major pathological sites for Huntington's disease, in p53+/+ but not the isogenic p53-/- mice. These results demonstrate that p53 protein can regulate huntingtin expression at transcriptional level, and suggest that a p53 stress response could be a modulator of the process of Huntington's disease.
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Registered trials
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.