Tseng Y T, Waschek J A, Padbury J F
Department of Pediatrics, Women and Infants' Hospital of Rhode Island, Brown University, Providence, USA.
Biochem Biophys Res Commun. 1995 Oct 13;215(2):606-12. doi: 10.1006/bbrc.1995.2507.
Functional data for the promoter of the beta 1-adrenergic receptor (beta 1AR) gene are lacking. We previously cloned the ovine beta 1AR gene and mapped the transcription start sites. We now report data on ovine beta 1AR gene expression obtained by transient transfection. Progressive deletion of upstream 5' flanking region moderately increased transcription activity in three cell lines compared to the full-length promoter. Deletion of sequences between -1530 and -953 produced the greatest increase in transcriptional activity. This region encompassed a putative GRE and an AP1 site. Deletion of the transcription start sites eliminated nearly all of the activity. Dexamethasone significantly increased activity of each of the promoter constructs tested in C6 glioma cells and an embryonic myocardial cell line, W1 cells. T3 alone had no effect and cotreatment with T3 did not augment the effects of dexamethasone. We conclude, basal transcription activity is repressed by a mechanism which operates through element(s) in the proximal promoter. Glucocorticoids increase transcription through mechanism(s) within the same region. We speculate that this region in the ovine beta 1AR promoter may be responsible for its unique transcription regulation.
β1 - 肾上腺素能受体（β1AR）基因启动子的功能数据尚缺。我们先前克隆了绵羊β1AR基因并确定了转录起始位点。我们现在报告通过瞬时转染获得的绵羊β1AR基因表达的数据。与全长启动子相比，上游5'侧翼区域的逐步缺失适度增加了三种细胞系中的转录活性。-1530至-953之间序列的缺失使转录活性增加最大。该区域包含一个假定的糖皮质激素反应元件（GRE）和一个AP1位点。转录起始位点的缺失几乎消除了所有活性。地塞米松显著增加了在C6胶质瘤细胞和胚胎心肌细胞系W1细胞中测试的每个启动子构建体的活性。单独的T3没有作用，并且与T3共同处理并未增强地塞米松的作用。我们得出结论，基础转录活性受到一种通过近端启动子中的元件起作用的机制的抑制。糖皮质激素通过同一区域内的机制增加转录。我们推测绵羊β1AR启动子中的该区域可能负责其独特的转录调控。
