The expression of the GLUT2 glucose transporter gene in liver is suppressed in cultured hepatoma cell lines and primary cultured hepatocytes. Earlier report showed that CCAAT/enhancer binding protein (C/EBP) regulates the promoter activity of the rat GLUT2 glucose transporter gene in liver cells. C/EBPalpha and C/EBPbeta activated the promoter activity by binding to at least two regions of the promoter and one of the C/EBP binding sites, named as site F, also has the AP-1 binding consensus. In this study, we investigated whether the AP-1 can influence on C/EBP binding to this site. The addition of recombinant c-Jun protein with liver extract caused the attenuation of C/EBP binding to site F with the appearance of a new shifted band. The shifted band was competed out with the addition of unlabeled AP-1 consensus oligonucleotide, indicating that c-Jun also can bind to site F. Another C/EBP site on GLUT2 promoter, site H, did not bind AP-1. Analysis of the DNA-protein complex revealed that C/EBP and c-Jun bind to site F in mutually exclusive manner rather than form heterodimeric complex with each other. From these results, it is suggested that the transcriptional activation of C/EBP may be influenced by c-Jun protein in certain status of the liver cells, such as acute phase response, as well as hepatocarcinogenesis.

中文翻译：

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在体外，c-Jun减弱了对大鼠GLUT2葡萄糖转运蛋白基因启动子的F位的C / EBP结合活性。

在培养的肝癌细胞系和原代培养的肝细胞中，肝脏中GLUT2葡萄糖转运蛋白基因的表达受到抑制。较早的报道表明，CCAAT /增强子结合蛋白（C / EBP）调节大鼠GLUT2葡萄糖转运蛋白基因在肝细胞中的启动子活性。C / EBPalpha和C / EBPbeta通过与启动子的至少两个区域结合来激活启动子活性，并且一个C / EBP结合位点（称为位点F）也具有AP-1结合共识。在这项研究中，我们调查了AP-1是否可以影响C / EBP结合该位点。肝提取物中加入重组c-Jun蛋白会导致C / EBP与位点F的结合减弱，并出现新的移位谱带。通过添加未标记的AP-1共有寡核苷酸，竞争了带区，这表明c-Jun也可以与位点F结合。GLUT2启动子上的另一个C / EBP位点，即位点H，未结合AP-1。DNA-蛋白质复合物的分析表明，C / EBP和c-Jun以互斥的方式与位点F结合，而不是彼此形成异二聚体复合物。从这些结果表明，在肝细胞的某些状态下，例如急性期反应以及肝癌的发生，C / EBP的转录激活可能受到c-Jun蛋白的影响。