PDF(Sci-hub)
Abstract：
The growth-regulated vimentin gene contains a functional double AP-1 binding site formed by two nearly perfect inverted repeats. We present evidence for down-regulation of vimentin expression by the retinoic acid receptor (RAR) in two mesodermally derived cell types. By mutation analysis we prove that the double consensus element is responsible for this negative regulation. From in vitro protein-DNA interaction studies we conclude that AP-1 binding is inhibited at RAR amounts required for occupation of the cognate RAR binding site in nuclear extracts from 3T3 cells and differentiated embryonal carcinoma cells. Furthermore, we show that, unlike in other cases, trans-activation of the vimentin AP-1 enhancer element can occur in undifferentiated embryonal carcinoma cells, despite the low amount of Jun and Fos proteins present in these cells. Here, however, down-regulation by retinoic acid cannot be detected.
摘要：
生长调节的波形蛋白基因包含由两个几乎完美的反向重复序列形成的功能性双AP-1结合位点。我们提供了两种中胚层衍生细胞类型中视黄酸受体（RAR）下调波形蛋白表达的证据。通过突变分析，我们证明了双重共识元件是这种负调控的原因。从体外蛋白质-DNA相互作用研究中，我们得出结论，在3T3细胞和分化的胚胎癌细胞的核提取物中占据同源RAR结合位点所需的RAR量下，AP-1结合受到抑制。此外，我们证明，与其他情况不同，波形蛋白AP-1增强子元件的反式激活可以发生在未分化的胚胎癌细胞中，尽管这些细胞中存在少量的Jun和Fos蛋白。这里,然而,不能检测到视黄酸的下调。
