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首页> 外文期刊>Molecular and Cellular Endocrinology >Androgen receptor signalling: comparative analysis of androgen response elements and implication of heat-shock protein 90 and 14-3-3eta.
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Androgen receptor signalling: comparative analysis of androgen response elements and implication of heat-shock protein 90 and 14-3-3eta.

机译：雄激素受体信号传导：雄激素反应元件的比较分析和热激蛋白90和14-3-3eta的含义。

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Androgen receptor (AR) signalling was analysed using as models the cysteine-rich secretory protein-1 (CRISP-1) and CRISP-3 gene promoters, which are differentially regulated by androgen in vivo and contain multiple potential androgen response elements. Using electrophoretic mobility shift assay, we identified several elements with differing affinities for the AR at positions -3706, -1270, -1253 and -350 of the CRISP-1 promoter and at positions -369 and -349 of the CRISP-3 promoter. The strongest binding was observed for the -1253 element of CRISP-1. In transactivation assays using a PC-3 cell line stably transfected with the AR (PC-3/AR), the -1253 element placed as two or four copies upstream of the TK minimal promoter yielded a strong induction of luciferase reporter gene activity in the presence of the androgen methyltrienolone (R1881). In the context of the CRISP promoters a 2-fold induction by R1881 was measured for the CRISP-3 upstream region whereas only limited effects were noted for the CRISP-1 upstream region. The androgenic stimulation of the p(-1253 ARE)(4x)-TK-luciferase reporter construct was dose-dependently inhibited by geldanamycin and radicicol, two compounds that selectively interact with the chaperone protein, heat-shock protein 90. Cotransfection with an expression vector for the 14-3-3eta protein markedly enhanced the androgen-dependent stimulation. These results emphasize the influence of promoter context on androgen regulation and the importance of AR-associated proteins.
机译：使用富含半胱氨酸的分泌蛋白-1（CRISP-1）和CRISP-3基因启动子作为模型分析了雄激素受体（AR）信号传导，它们在体内受到雄激素的调节，并包含多种潜在的雄激素反应元件。使用电泳迁移率漂移分析，我们在CRISP-1启动子的-3706，-1270，-1253和-350位置以及CRISP-3启动子的-369和-349位置鉴定了几种具有不同亲和力的元素。对于CRISP-1的-1253元件观察到最强的结合。在使用被AR稳定转染的PC-3细胞系（PC-3 / AR）进行的转激活试验中，位于TK最小启动子上游2或4个拷贝的-1253元件在荧光素酶报告基因活性中产生了强烈的诱导作用。雄激素甲基三烯酮（R1881）的存在。在CRISP启动子的情况下，对于CRISP-3上游区域，测量了R1881的2倍诱导，而对于CRISP-1上游区域，仅观察到有限的作用。 p（-1253 ARE）（4x）-TK-萤光素酶报告基因构建体的雄激素刺激受到格尔德霉素和radicicol的剂量依赖性抑制，这两种化合物与伴侣蛋白，热激蛋白90选择性相互作用。与一种表达共转染14-3-3eta蛋白的载体显着增强了雄激素依赖性刺激。这些结果强调了启动子环境对雄激素调节的影响以及AR相关蛋白的重要性。

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