人胃抑制性多肽基因启动子区域中的两个3'，5'-环磷酸腺苷反应元件。
Two 3',5'-cyclic-adenosine monophosphate response elements in the promoter region of the human gastric inhibitory polypeptide gene.
作者信息
Someya Y, Inagaki N, Maekawa T, Seino Y, Ishii S
机构信息
Department of Medicine, Kyoto University School of Medicine, Japan.
出版信息
FEBS Lett. 1993 Feb 8;317(1-2):67-73. doi: 10.1016/0014-5793(93)81493-j.
Transfection of chimeric chloramphenicol acetyltransferase plasmids containing various deletions of the human gastric inhibitory polypeptide (GIP) promoter into hamster insulinoma (HIT T15) cells indicated that the region between -180 and +14 is sufficient for basal promoter activity. Two CRE-BP1 binding sites were identified in this promoter region by DNase I footprinting with the bacterially expressed cAMP response element (CRE) binding protein, CRE-BP1. Mutation analyses showed that these two CREs are required for the basal promoter activity, and furthermore that one site, at nucleotide-158, contributed mainly to the cAMP inducibility of the GIP promoter in HIT T15 cells. Interestingly, the GIP promoter activity was repressed by the c-jun proto-oncogene product, possibly through the CREs.
将含有不同缺失的人胃抑制性多肽（GIP）启动子的嵌合氯霉素乙酰转移酶质粒转染到仓鼠胰岛素瘤（HIT T15）细胞中，结果表明 -180 至 +14 之间的区域足以支持基础启动子活性。通过用细菌表达的环磷酸腺苷反应元件（CRE）结合蛋白 CRE-BP1 进行 DNase I 足迹分析，在该启动子区域鉴定出两个 CRE-BP1 结合位点。突变分析表明，这两个 CRE 对于基础启动子活性是必需的，此外，位于核苷酸 -158 的一个位点主要促成了 HIT T15 细胞中 GIP 启动子的环磷酸腺苷诱导性。有趣的是，GIP 启动子活性可能通过 CRE 被 c-jun 原癌基因产物抑制。
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