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雌激素受体α(ERα)是一种配体诱导型的转录调节因子,作用机制是与配体结合后形成复合物,然后与靶基因启 动子区特定序列-雌激素反应元件结合。通过这种方式调节的因子有pS2、组织蛋白酶、卵黄生成素、c-fos、c-jun、bcl-2、腺苷脱氨酶、TGF-α和tPA等;近期又发现ERα与配体形成的复合物通过其他转录因子如AP1间接作用于靶基因。通过上述方式ERα的配体(ER激动剂和拮抗剂)发挥各自的促进和抑制细胞分裂作用。但上述理论并不能完全解释ERα作用,向ERα(-)的CHO和HeLa细胞内转导ERα基因并表达ERα蛋白,E_2不但不能促进细胞生长反而抑制生长甚至引
Estrogen receptor alpha (ERa) is a ligand-inducible transcriptional regulator that acts by binding to ligands to form complexes that then bind to estrogen-responsive elements, a specific sequence in the promoter region of the target gene. Factors regulated in this way are pS2, cathepsin, vitellogenin, c-fos, c-jun, bcl-2, adenosine deaminase, TGF- and tPA; recently also found that ERα and ligand formation Complex indirectly acts on the target gene through other transcription factors such as AP1. The ERα ligands (ER agonists and antagonists) exert their respective promotion and inhibition of cell division by the above-mentioned means. However, the above theory does not completely explain the role of ERα, ERα gene expression in ERα (-) CHO and HeLa cells and expression of ERα protein, E_2 not only can not promote cell growth but even inhibit growth