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首页> 外文期刊>The Journal of Nutritional Biochemistry >Nuclear receptor binding to the retinoic acid response elements of the phosphoenolpyruvate carboxykinase gene in vivo: effects of vitamin A deficiency
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Nuclear receptor binding to the retinoic acid response elements of the phosphoenolpyruvate carboxykinase gene in vivo: effects of vitamin A deficiency

机译：核受体结合到体内磷酸烯醇丙酮酸羧激酶基因的视黄酸反应元件：维生素A缺乏症的影响

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摘要

Vitamin A deficiency decreases hepatic phosphoenolpyruvate carboxykinase (PEPCK) gene expression in mice and expression is restored with retinoic acid treatment in vivo. This report examines further the mechanism of retinoid regulation of the PEPCK gene in vivo. We have identified nuclear receptors that bind to retinoic acid response elements (RAREs) in the PEPCK promoter by electrophoretic mobility shift assay and have verified these in vivo using chromatin immunoprecipitation (ChIP) in mouse liver. Based on the results of our ChIP assay, hepatic nuclear factor (HNF)-4alpha, retinoid X receptor (RXR) alpha, retinoic acid receptor (RAR) alpha, peroxisome proliferator-activated receptor (PPAR) alpha and chicken ovalbumin upstream promoter transcription factor (COUP-TF) II bind to the downstream retinoic acid response unit RARE1/RARE2, and PPARalpha and RXRalpha bind to the upstream RARE3 of the PEPCK gene. HNF-4alpha, RXRalpha, RARalpha, PPARalpha and COUP-TFII bind PEPCK RAREs in a specific pattern that, with the exception of PPARalpha, does not change significantly with vitamin A deficiency. PPARalpha binding to the upstream retinoic acid response element is decreased in the vitamin A-deficient liver, when compared to the vitamin A-sufficient state. These results provide the first in vivo measures of nuclear receptor binding to the upstream and downstream RAREs of the PEPCK gene under conditions where the nucleosomal structure of the chromatin is maintained and the nuclear receptors are physically cross-linked in situ to the PEPCK DNA in intact liver.
机译：维生素A缺乏症会降低小鼠肝磷酸烯醇丙酮酸羧化激酶（PEPCK）基因的表达，并在体内通过视黄酸处理恢复其表达。该报告进一步检查了类维生素A调节体内PEPCK基因的机制。我们已经通过电泳迁移率变动分析确定了与PEPCK启动子中的视黄酸应答元件（RARE）结合的核受体，并已在小鼠肝脏中使用染色质免疫沉淀（ChIP）在体内验证了这些受体。根据我们ChIP分析的结果，肝核因子（HNF）-4alpha，类维生素A X受体（RXR）α，视黄酸受体（RAR）α，过氧化物酶体增殖物激活受体（PPAR）α和鸡卵清蛋白上游启动子转录因子（COUP-TF）II与下游视黄酸应答单元RARE1 / RARE2结合，PPARalpha和RXRalpha与PEPCK基因的上游RARE3结合。 HNF-4alpha，RXRalpha，RARalpha，PPARalpha和COUP-TFII以特定​​的模式与PEPCK RARE结合，除了PPARalpha之外，维生素C缺乏症不会明显改变。与维生素A充足的状态相比，维生素A缺乏的肝脏中PPARalpha与上游视黄酸响应元件的结合降低。这些结果提供了在染色质的核小体结构得以维持且核受体在原位与PEPCK DNA完好无损地物理交联的条件下，核受体与PEPCK基因的上游和下游RARE结合的首次体内测量。肝。

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