کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1940063 | 1050773 | 2006 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Histone deacetylase inhibitor apicidin induces cyclin E expression through Sp1 sites Histone deacetylase inhibitor apicidin induces cyclin E expression through Sp1 sites](/preview/png/1940063.png)
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.
Journal: Biochemical and Biophysical Research Communications - Volume 342, Issue 4, 21 April 2006, Pages 1168–1173