Takata Yutaka, Takeda Shigeki, Kawanami Takako, Takiguchi Soichi, Yoshida Yuki, Miyasaka Kyoko, Funakoshi Akihiro
Department of Gastroenterology, National Kyushu Cancer Center, 3-1-1 Notame, Minami-ku, Fukuoka 811-1395, Japan.
J Gastroenterol. 2002;37(10):815-20. doi: 10.1007/s005350200135.
Background. We have previously shown that polymorphism in the promoter region of the human cholecystokinin type-A receptor ( CCKAR) gene is a genetic factor affecting obesity. However, there have not yet been any reports of analysis of the promoter activity of CCKAR genes, and thus almost nothing is known about CCKAR transcriptional regulation. Methods. Using STC-1 cells, an enteroendocrine tumor cell line, we measured the promoter activity of the human CCKAR gene by a transient transfection method. Results. We showed that STC-1 cells expressed CCKAR as well as its peptide-ligand, CCK. Analysis of a series of 5'-deleted promoter constructs showed that the proximal 622-base region upstream from the initiation site, which contained two GC-box motifs, was important as a regulatory region for the transcriptional activity. However, no significant differences were found for the promoter activities of polymorphic promoter constructs. Conclusions. These results suggest that the reported polymorphism may not play a role in transcriptional regulation.
背景。我们之前已经表明，人类A型胆囊收缩素受体（CCKAR）基因启动子区域的多态性是影响肥胖的一个遗传因素。然而，尚未有关于CCKAR基因启动子活性分析的报道，因此对CCKAR转录调控几乎一无所知。方法。使用肠内分泌肿瘤细胞系STC-1细胞，我们通过瞬时转染法测量了人类CCKAR基因的启动子活性。结果。我们发现STC-1细胞表达CCKAR及其肽配体CCK。对一系列5'-缺失启动子构建体的分析表明，起始位点上游近端622个碱基区域，包含两个GC盒基序，作为转录活性的调控区域很重要。然而，多态性启动子构建体的启动子活性未发现显著差异。结论。这些结果表明，所报道的多态性可能在转录调控中不起作用。
