共查询到20条相似文献,搜索用时 359 毫秒
1.
Piech-Dumas KM Best JA Chen Y Nagamoto-Combs K Osterhout CA Tank AW 《Journal of neurochemistry》2001,76(5):1376-1385
Tyrosine hydroxylase (TH) gene promoter activity is increased in PC12 cells that are treated with the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA). Mutagenesis of either the cAMP responsive element (CRE) or the activator protein-1 element (AP1) within the TH gene proximal promoter leads to a dramatic inhibition of the TPA response. The TH CRE and TH AP1 sites are also independently responsive to TPA in minimal promoter constructs. TPA treatment results in phosphorylation of cAMP responsive element binding protein (CREB) and activation of cAMP-dependent protein kinase (PKA) in PC12 cells; hence, we tested whether CREB and/or PKA are essential for the TPA response. In CREB-deficient cells, the response of the full TH gene proximal promoter or the independent response of the TH CRE by itself to TPA is inhibited. The TPA-inducibility of TH mRNA is also blocked in CREB-deficient cells. Expression of the PKA inhibitor protein, PKI, also inhibits the independent response of the TH CRE to TPA. Our results support the hypothesis that TPA stimulates the TH gene promoter via signaling pathways that activate either the TH AP1 or TH CRE sites. Both signaling pathways are dependent on CREB and the TH CRE-mediated pathway is dependent on PKA. 相似文献
2.
3.
J R Grove P J Deutsch D J Price J F Habener J Avruch 《The Journal of biological chemistry》1989,264(33):19506-19513
4.
5.
6.
7.
为了研究 C B P在胰岛 H I T 细胞中调节基因转录的机制,将不同的 C B P片段瞬时转染到细胞中,观察其转录活性.实验表明,在胰岛 H I T 细胞中,膜去极化及 c A M P 均可诱导 C B P30( C R E B结合功能区)转录活性增强,并有协同效应. P K C对 C B P30 的转录活性无影响;与 C R E B有更强结合力的 C B P K I X S/ B(氨基酸序列短于 C B P30 的 C R E B结合功能区)其基本转录活性及膜去极化、c A M P诱导下的转录活性均比 C B P30 更强.反义 C R E B 的过度表达可降低 c A M P诱导的 C B P的转录活性.提示在胰岛 H I T 细胞中,膜去极化及 c A M P对共转录因子 C B P转录活性的调节作用通过 C R E B介导. 相似文献
8.
在胰岛细胞株 H I T 细胞中,用瞬时转染法观察高 K+ 导致的膜去极化与c A M P对 C B P C端片段转录活性的影响.发现二者均可诱导 C B P C端片段的转录活性增强,并有协同效应; C B P C端片段的突变体( Ser 1 772 突变为 Ala)表现相同的诱导特性,但其基本转录活性降低.说明膜去极化和 c A M P对 C B P C 端片段转录活性的诱导作用与 P K A 磷酸化位点 Ser 1 772 无关,而该位点的磷酸化对调节 C B P C 端片段的基本转录活性起重要作用.蛋白激酶 C 通路对 C B P Ti的转录活性无影响. 相似文献
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.