ArticleArchives of biochemistry and biophysics2009
p53 regulates Hsp90beta during arsenite-induced cytotoxicity in glutathione-deficient cells.
Article in Archives of biochemistry and biophysics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- The Hsp90β Isoform: An Attractive Target for Drug Development.Medicinal research reviews · 2025Review
- Heat shock protein 90-mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells.Molecular biology of the cell · 2011Article
- One function--multiple mechanisms: the manifold activities of p53 as a transcriptional repressor.Journal of biomedicine & biotechnology · 2011Review
- Arsenite causes down-regulation of Akt and c-Fos, cell cycle dysfunction and apoptosis in glutathione-deficient cells.Journal of cellular biochemistry · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
p53, a tumor suppressor and transcription factor, is a critical modulator in the cellular response to stress. Exposure of glutathione-deficient GCS-2 cells to arsenite significantly phosphorylated and stabilized p53. In addition, p53 transcriptionally repressed Hsp90beta gene expression. Mutation analysis revealed a p53 binding site in the 5' flanking region responsible for the regulation of Hsp90beta gene. Electrophoretic mobility shift assay showed that p53 is bound to Hsp90beta promoter region. ATM kinase, a major determinant in the modulation of p53 specifically affected its phosphorylation at Ser-15. ATM kinase-mediated phosphorylation of p53 is regulated through phosphorylation of Chk2. Down-regulation of ATM and Chk2 by their small interfering RNAs (siRNAs) attenuated the arsenite-induced phosphorylation of p53 and restored Hsp90beta mRNA levels. Taken together, these findings suggest that arsenite acts through ATM and Chk2 to induce phosphorylation of p53. This results in the transcriptional repression of Hsp90beta, under GSH-deficient conditions which may play a role in arsenic-mediated pathogenesis.
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Registered trials
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