Moore B A, Miskimins R, Miskimins W K
Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, Vermillion 57069, USA.
Mol Cell Biol Res Commun. 1999 Apr;1(1):1-6. doi: 10.1006/mcbr.1999.0100.
We have found that the transferrin receptor gene promoter is strongly activated by exposure of B16 melanoma cells to UV light. This is a delayed event occurring more than 6 h after exposure and requires an AP-1/CRE-like element in the promoter as demonstrated by site-specific mutagenesis. UV irradiation enhances the binding of a nuclear factor to this element and supershift analysis demonstrates that this DNA-protein complex involves ATF-1. No other members of either the AP-1 or CREB/ATF families of transcription factors were found to bind to this DNA element in UV-irradiated B16 cells. Western blots show that the level of ATF-1 does not change following exposure to UV light, indicating that the increased binding of this factor is most likely mediated by posttranslational modifications in response to UV-mediated signaling pathways.
我们发现,将B16黑色素瘤细胞暴露于紫外线下可强烈激活转铁蛋白受体基因启动子。这是一个延迟事件,发生在暴露后6小时以上,并且如位点特异性诱变所示,需要启动子中的一个AP-1/CRE样元件。紫外线照射增强了一种核因子与该元件的结合,超迁移分析表明这种DNA-蛋白质复合物涉及ATF-1。在紫外线照射的B16细胞中,未发现转录因子AP-1或CREB/ATF家族的其他成员与该DNA元件结合。蛋白质免疫印迹显示,暴露于紫外线下后,ATF-1的水平没有变化,这表明该因子结合增加很可能是由响应紫外线介导的信号通路的翻译后修饰介导的。