Progesterone induction of metallothionein-IIA gene expression.
Progesterone induction of metallothionein-IIA gene expression.
复制标题
黄体酮诱导金属硫蛋白-IIA 基因表达。
作者：
E. Slater;A. Cato;M. Karin;J. Baxter;M. Beato
金属硫蛋白基因的表达是已知的由糖皮质激素在多种细胞诱导。本研究表明，在含有功能性孕酮受体的人细胞系中，内源性金属硫蛋白iia （hMTIIA）基因可被合成孕激素R5020和醋酸羟孕酮诱导。我们发现部分纯化的黄体酮受体在体外与该基因的启动子区域结合，这一发现支持了这种效应反映了与金属硫蛋白基因的直接相互作用。在孕激素受体的甲基化研究中，dna酶I足迹和鸟嘌呤残基的保护范围与先前对糖皮质激素受体的描述相似。因此，人金属硫蛋白iia基因的激素调控元件可以介导糖皮质激素和孕激素的调控，小鼠乳腺肿瘤病毒的激素调控元件也可以。
Expression of the metallothionein gene is known to be induced by glucocorticoids in a variety of cells. Here we show that in human cell lines containing functional progesterone receptors, the endogenous metallothionein-IIA (hMTIIA) gene is inducible by the synthetic progestins R5020 and medroxy-progesterone acetate. That this effect reflects a direct interaction with the metallothionein gene is supported by our finding that the partially purified progesterone receptor binds to the promoter region of the gene in vitro. The limits of the DNase I footprint and the guanine residues protected in methylation studies with the progesterone receptor are similar to those previously described for the glucocorticoid receptor. Thus, the hormone regulatory element of the human metallothionein-IIA gene can mediate regulation by both glucocorticoids and progestins, as does the hormone regulatory element of mouse mammary tumor virus.