ArticleThe Journal of biological chemistry2013
TAp73 protein stability is controlled by histone deacetylase 1 via regulation of Hsp90 chaperone function.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Isoform-specific disruption of theeLife · 2023Article
- TP73 Isoform-specific disruption reveals a critical role of TAp73beta in growth suppression and inflammatory response.Cell death & disease · 2023Article
- Functional stratification of cancer drugs through integrated network similarity.NPJ systems biology and applications · 2022Article
- Review
- Post-translational modifications of Hsp90 and translating the chaperone code.The Journal of biological chemistry · 2020Review
- Mutant p53 antagonizes p63/p73-mediated tumor suppression via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Histone deacetylase activity mediates acquired resistance towards structurally diverse HSP90 inhibitors.Molecular oncology · 2017Article
- LSD1 engages a corepressor complex for the activation of the estrogen receptor α by estrogen and cAMP.Nucleic acids research · 2016Article
- ΔNp63/DGCR8-Dependent MicroRNAs Mediate Therapeutic Efficacy of HDAC Inhibitors in Cancer.Cancer cell · 2016Article
- A balancing act: orchestrating amino-truncated and full-length p73 variants as decisive factors in cancer progression.Oncogene · 2015Review
- Hsp90, the concertmaster: tuning transcription.Frontiers in oncology · 2015Review
- Eradication of metastatic melanoma through cooperative expression of RNA-based HDAC1 inhibitor and p73 by oncolytic adenovirus.Oncotarget · 2014Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) play important roles in fundamental cellular processes, and HDAC inhibitors are emerging as promising cancer therapeutics. p73, a member of the p53 family, plays a critical role in tumor suppression and neural development. Interestingly, p73 produces two classes of proteins with opposing functions: the full-length TAp73 and the N-terminally truncated ΔNp73. In the current study, we sought to characterize the potential regulation of p73 by HDACs and found that histone deacetylase 1 (HDAC1) is a key regulator of TAp73 protein stability. Specifically, we showed that HDAC1 inhibition by HDAC inhibitors or by siRNA shortened the half-life of TAp73 protein and subsequently decreased TAp73 expression under normal and DNA damage-induced conditions. Mechanistically, we found that HDAC1 knockdown resulted in hyperacetylation and inactivation of heat shock protein 90, which disrupted the interaction between heat shock protein 90 and TAp73 and thus promoted the proteasomal degradation of TAp73. Functionally, we found that down-regulation of TAp73 was required for the enhanced cell migration mediated by HDAC1 knockdown. Together, we uncover a novel regulation of TAp73 protein stability by HDAC1-heat shock protein 90 chaperone complex, and our data suggest that TAp73 is a critical downstream mediator of HDAC1-regulated cell migration.
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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.