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首页> 外文期刊>American Journal of Physiology >Regulation of the Na-K-ATPase beta(1)-subunit promoter by multiple prostaglandin-responsive elements.
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Regulation of the Na-K-ATPase beta(1)-subunit promoter by multiple prostaglandin-responsive elements.

机译：Na-K-ATPase beta（1）-亚基启动子的调节由多个前列腺素响应元件。

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摘要

Renal prostaglandins modulate the activity of a number of the transport systems in the kidney, including the Na-K-ATPase. Not only do prostaglandins have acute affects on renal Na-K-ATPase, but in addition prostaglandins have chronic affects, which include regulation at the transcriptional level. Previously, we have presented evidence that one such prostaglandin, PGE(1), stimulates the transcription of the human Na-K-ATPase beta(1)-subunit gene in Madin-Darby canine kidney cells via cAMP- and Ca(2+)-mediated pathways (Taub M, Borsick M, Geisel J, Matlhagela K, Rajkhowa T, and Allen C. Exp Cell Res 299: 1-14, 2004; Matlhagela K, Borsick M, Rajkhowa T, and Taub M. J Biol Chem 280: 334-346, 2005). Evidence was presented indicating that PGE(1) stimulation was mediated through the binding of cAMP-regulatory element binding protein (CREB) to a prostaglandin-responsive element (PGRE) as well as Sp1 binding to an adjacent Sp1 site. In this report, we present evidence from EMSAs and DNA affinity precipitation studies that another PGRE present in the Na-K-ATPase beta(1)-subunit promoter similarly binds CREB and Sp1. The evidence that indicates a requirement for CREB as well as Sp1 for gene activation through both PGREs (PGRE1 and PGRE3) includes studies with a dominant negative CREB (KCREB), Drosophila SL2 cells, and PGRE mutants. The results of these studies are indicative of a synergism between Sp1 and CREB in mediating regulation by PGRE3; while regulation occurring through PGRE1 also involves Sp1 and CREB, the mechanism appears to be distinct.
机译：肾前列腺素调节肾脏中许多运输系统的活性，包括Na-K-ATPase。前列腺素不仅对肾Na-K-ATP酶有急性影响，而且前列腺素还具有慢性影响，包括在转录水平上的调节。以前，我们已经提供了证据，证明这样的前列腺素PGE（1）通过cAMP-和Ca（2+）刺激Madin-Darby犬肾细胞中人Na-K-ATPase beta（1）-亚基基因的转录。介导的途径（Taub M，Borsick M，Geisel J，Matlhagela K，Rajkhowa T和Allen C.Exp Cell Res 299：1-14，2004; Matlhagela K，Borsick M，Rajkhowa T和Taub M.J Biol Chem 280：334-346，2005）。证据表明，PGE（1）刺激是通过cAMP调节元件结合蛋白（CREB）与前列腺素反应元件（PGRE）的结合以及Sp1与相邻Sp1位点的结合介导的。在此报告中，我们提供了来自EMSA和DNA亲和沉淀研究的证据，即Na-K-ATPase beta（1）-亚基启动子中存在的另一个PGRE类似地结合了CREB和Sp1。表明通过两个PGRE（PGRE1和PGRE3）激活基因需要CREB和Sp1的证据包括对显性阴性CREB（KCREB），果蝇SL2细胞和PGRE突变体的研究。这些研究的结果表明Sp1和CREB在PGRE3介导的调控中具有协同作用。尽管通过PGRE1进行的调控还涉及Sp1和CREB，但其机制似乎不同。

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