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首页> 外文期刊>Molecular and Cellular Biology >Regulatory role of MEF2D in serum induction of the c-jun promoter.
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Regulatory role of MEF2D in serum induction of the c-jun promoter.

机译：MEF2D在c-jun启动子的血清诱导中的调节作用。

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Serum induction of c-jun expression in HeLa cells requires a MEF2 site at -59 in the c-jun promoter. MEF2 sites, found in many muscle-specific enhancers, are bound by a family of transcription factors, MEF2A through -D, which are related to serum response factor in their DNA binding domains. We have found that MEF2D is the predominant protein in HeLa cells that binds to the c-jun MEF2 site. Serum induction of a MEF2 reporter gene was not observed in a line of NIH 3T3 cells which contain low MEF2 site binding activity. Transfection of MEF2D into NIH 3T3 cells reconstituted serum induction, demonstrating that MEF2D is required for the serum response. Deletion analysis of MEF2D showed that its DNA binding domain, when fused to a heterologous transcriptional activation domain, was sufficient for serum induction of a MEF2 reporter gene. This is the domain homologous to that in the serum response factor which is required for serum induction of the c-fos serum response element, suggesting that serum regulation of c-fos and c-jun may share a common mechanism.
机译：血清在HeLa细胞中诱导c-jun表达需要在c-jun启动子中位于-59的MEF2位点。在许多肌肉特异性增强子中发现的MEF2位点被一系列转录因子MEF2A至-D结合，这些转录因子在其DNA结合域中与血清反应因子有关。我们发现，MEF2D是HeLa细胞中与c-jun MEF2位点结合的主要蛋白质。在含有低MEF2位点结合活性的NIH 3T3细胞系中未观察到血清对MEF2报道基因的诱导。将MEF2D转染到NIH 3T3细胞中可重新构成血清诱导，这表明MEF2D是血清反应所必需的。对MEF2D的缺失分析表明，当其DNA结合结构域与异源转录激活结构域融合时，足以用于血清诱导MEF2报道基因。这是与血清诱导c-fos血清反应元件所需的血清反应因子中的域同源的域，这表明c-fos和c-jun的血清调节可能具有共同的机制。

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