Klein-Hitpass L, Ryffel G U, Heitlinger E, Cato A C
Kernforschungszentrum Karlsruhe, Institut für Genetik und Toxikologie, FRG.
Nucleic Acids Res. 1988 Jan 25;16(2):647-63. doi: 10.1093/nar/16.2.647.
Sequences located upstream of the transcription initiation site of the Xenopus vitellogenin A2 (vit A2) gene contain a hormone dependent enhancer that confers estrogen control to the heterologous thymidine kinase (tk) promoter. As a minimal functional estrogen responsive element (ERE), we have defined the 13 bp palindrome GGTCACAGTGACC. This ERE binds estrogen receptor preferentially in vitro. Although the ERE shares some structural features with the glucocorticoid responsive element (GRE) it is distinct from this element since it neither binds glucocorticoid receptor in vitro nor does it confer glucocorticoid inducibility to a fusion gene. Point mutations within the ERE decrease its affinity for the estrogen receptor and result in a complete loss of estrogen inducibility.
非洲爪蟾卵黄蛋白原A2(vit A2)基因转录起始位点上游的序列包含一个激素依赖性增强子,该增强子可将雌激素调控赋予异源胸苷激酶(tk)启动子。作为最小功能雌激素反应元件(ERE),我们确定了13bp的回文序列GGTCACAGTGACC。该ERE在体外优先结合雌激素受体。尽管ERE与糖皮质激素反应元件(GRE)具有一些结构特征,但它与该元件不同,因为它在体外既不结合糖皮质激素受体,也不赋予融合基因糖皮质激素诱导性。ERE内的点突变会降低其对雌激素受体的亲和力,并导致雌激素诱导性完全丧失。