Mosselman S, Höppener J W, de Wit L, Soeller W, Lips C J, Jansz H S
Institute of Molecular Biology and Medical Biotechnology, Utrecht, The Netherlands.
FEBS Lett. 1990 Oct 1;271(1-2):33-6. doi: 10.1016/0014-5793(90)80365-p.
Aberrant expression of the islet amyloid polypeptide (IAPP) gene might be involved in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Here, we report that IAPP promoter-luciferase constructs revealed tissue-specific activity. This activity was not mediated by cAMP. Sequential 5' deletions of the IAPP promoter caused a progressive derepression of the IAPP gene promoter in IAPP-producing cells. Comparison of the nucleotide sequence of the IAPP promoter with that of the insulin promoter (both active in pancreatic beta-cells) reveals two sequence elements of putative importance: an insulin enhancer-like sequence and an element which corresponds to a protected domain in rat insulin I gene promoter footprint experiments.
胰岛淀粉样多肽(IAPP)基因的异常表达可能参与非胰岛素依赖型糖尿病(NIDDM)的发病机制。在此,我们报告IAPP启动子-荧光素酶构建体显示出组织特异性活性。这种活性不是由cAMP介导的。IAPP启动子的5'端连续缺失导致IAPP产生细胞中IAPP基因启动子的逐渐去抑制。将IAPP启动子的核苷酸序列与胰岛素启动子(两者在胰腺β细胞中均有活性)的核苷酸序列进行比较,发现两个可能具有重要意义的序列元件:一个胰岛素增强子样序列和一个与大鼠胰岛素I基因启动子足迹实验中的一个保护结构域相对应的元件。