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  • Title: Histone deacetylase inhibitor apicidin induces cyclin E expression through Sp1 sites.
    Author: Kim S, Kang JK, Kim YK, Seo DW, Ahn SH, Lee JC, Lee CH, You JS, Cho EJ, Lee HW, Han JW.
    Journal: Biochem Biophys Res Commun; 2006 Apr 21; 342(4):1168-73. PubMed ID: 16516150.
    Abstract:
    We show that a histone deacetylase (HDAC) inhibitor apicidin increases the transcriptional activity of cyclin E gene, which results in accumulation of cyclin E mRNA and protein in a time- and dose-dependent manner. Interestingly, apicidin induction of cyclin E gene is found to be mediated by Sp1- rather than E2F-binding sites in the cyclin E promoter, as evidenced by the fact that specific inhibition of Sp1 leads to a decrease in apicidin activation of cyclin E promoter activity and protein expression, but mutation of E2F-binding sites of cyclin E promoter region fails to inhibit the ability of apicidin to activate cyclin E transcription. In addition, this transcriptional activation of cyclin E by apicidin is associated with histone hyperacetylation of cyclin E promoter region containing Sp1-binding sites. Our results demonstrate that regulation of histone modification by an HDAC inhibitor apicidin contributes to induction of cyclin E expression and this effect is Sp1-dependent.
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