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首页> 外文期刊>Molecular and Cellular Biology >Specificity of a retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter: consequences of both retinoic acid and thyroid hormone receptor binding.
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Specificity of a retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter: consequences of both retinoic acid and thyroid hormone receptor binding.

机译：磷酸烯醇丙酮酸羧激酶基因启动子中视黄酸反应元件的特异性：视黄酸和甲状腺激素受体结合的后果。

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摘要

The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Fusion gene constructs consisting of PEPCK promoter sequences ligated to the chloramphenicol acetyltransferase (CAT) reporter gene were used for this analysis. While T3 induced CAT expression to a small degree (about twofold) when such constructs were transiently transfected into H4IIE rat hepatoma cells, along with an expression vector encoding the alpha subtype of the T3 receptor (TR), this effect was mediated by promoter sequences distinct from the PEPCK RARE. Although TRs were capable of binding the PEPCK RARE in the form of putative monomers, dimers, and heterodimers with RA receptors (RARs), this element failed to mediate any positive effect of T3 on gene expression. In contrast, the PEPCK RARE mediated six- to eightfold induction of CAT expression by RA. When TRs were coexpressed along with RARs in transfected H4IIE cells, this RA induction was substantially blunted in a T3-independent manner. This inhibitory effect may be due to the binding of nonfunctional TRs or TR-RAR heterodimers to the PEPCK RARE. A model is proposed to explain the previously observed in vivo effects of T3 on PEPCK gene expression.
机译：研究了磷酸烯醇丙酮酸羧激酶（PEPCK）基因启动子中视黄酸（RA）反应元件（RARE）介导RA或甲状腺激素（T3）对基因表达的影响的能力。由连接到氯霉素乙酰基转移酶（CAT）报告基因的PEPCK启动子序列组成的融合基因构建体用于该分析。当将此类构建体瞬时转染到H4IIE大鼠肝癌细胞中时，T3会在某种程度上诱导CAT表达（大约两倍），以及编码T3受体（TR）的α亚型的表达载体，这种作用是由不同的启动子序列介导的从PEPCK RARE。尽管TR能够以假定的单体，二聚体和带有RA受体（RAR）的异二聚体的形式结合PEPCK RARE，但该元素未能介导T3对基因表达的任何积极影响。相反，PEPCK RARE介导了RA对CAT表达的六到八倍诱导。当TRs与RARs在转染的H4IIE细胞中共表达时，这种RA诱导基本上以T3独立的方式减弱了。这种抑制作用可能是由于非功能性TR或TR-RAR异二聚体与PEPCK RARE的结合所致。提出了一个模型来解释先前观察到的T3对PEPCK基因表达的体内作用。

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