Solomon S S, Palazzolo M R, Takahashi T, Raghow R
VAMC Research Service, Department of Medicine, University of Tennessee College of Medicine, Memphis, USA.
Endocrinology. 1997 Nov;138(11):5052-4. doi: 10.1210/endo.138.11.5648.
Insulin positively regulates transcription of rat calmodulin (CaM) I gene and activates the low Km cyclic AMP (cAMP) phosphodiesterase (PDE). To elucidate the mechanism of transcriptional regulation, rat hepatoma (H-411E) cells were transfected with DNA constructs containing the putative CaM promoters coupled to a luciferase reporter and challenged with insulin. Activation of the full length 1835 bp rat CaM I promoter containing all three Sp1 sites or truncated promoters with combinations of one to three of the Sp1 sites was studied in Sp1 deficient Drosophilia SL2 cells and in SL2 cells co-transfected with an Sp1 expression vector and re-challenged with insulin. Our results demonstrate that Sp1 is obligatory for basal activation of the CaM promoter. The maximal insulin stimulation of CaM promoter is elicited only if it contains at least two Sp1 sites.
胰岛素正向调节大鼠钙调蛋白（CaM）I基因的转录，并激活低Km环磷酸腺苷（cAMP）磷酸二酯酶（PDE）。为了阐明转录调控的机制，将含有推定的CaM启动子并与荧光素酶报告基因偶联的DNA构建体转染到大鼠肝癌（H - 411E）细胞中，并用胰岛素进行刺激。在缺乏Sp1的果蝇SL2细胞以及与Sp1表达载体共转染并再次用胰岛素刺激的SL2细胞中，研究了包含所有三个Sp1位点的全长1835 bp大鼠CaM I启动子或具有一至三个Sp1位点组合的截短启动子的激活情况。我们的结果表明，Sp1对于CaM启动子的基础激活是必不可少的。CaM启动子只有在至少包含两个Sp1位点时才能引发最大程度的胰岛素刺激。
