地塞米松介导的胰岛素受体mRNA稳定。

D Hines, V Hug, J R Levy
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引用次数: 11

摘要

为了确定糖皮质激素介导胰岛素受体(IR)基因表达增强的机制,我们将糖皮质激素受体表达载体和含有由MMTV或IR启动子驱动的报告基因的质粒共转染到COS 7细胞中。地塞米松(Dex)使MMTV启动子活性增加100%,但对IR启动子活性无影响。在糖皮质激素应答的乳腺癌细胞系中,MCF-7、Dex使IR mRNA增加了60%,并使IR mRNA的半衰期从大约6小时延长到> 24小时。胰岛素受体3'非翻译区不存在糖皮质激素应答元件。糖皮质激素稳定IR mRNA。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dexamethasone mediated stabilization of insulin receptor mRNA.

To determine the mechanism of glucocorticoid mediated enhancement of insulin receptor (IR) gene expression, we cotransfected a glucocorticoid receptor expression vector and a plasmid containing a reporter gene driven by an MMTV or IR promoter into COS 7 cells. Dexamethasone (Dex) increased MMTV promoter activity by 100% but had no effect on IR promoter activity. In the glucocorticoid responsive breast cancer cell line, MCF-7, Dex increased IR mRNA by 60%, and increased the IR mRNA half-life from approximately 6hrs to > 24 hrs. No glucocorticoid responsive element could be located in the insulin receptor 3' untranslated region. Glucocorticoids stabilize IR mRNA.

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