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首页> 外文期刊>Journal of cellular biochemistry. >Induction of Id2 expression by cardiac transcription factors GATA4 and Nkx2.5.
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Induction of Id2 expression by cardiac transcription factors GATA4 and Nkx2.5.

机译：心脏转录因子GATA4和Nkx2.5诱导Id2表达。

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摘要

Inhibitor of differentiation/DNA binding (Id) proteins function as a regulator of helix-loop-helix proteins participating in cell lineage commitment and differentiation. Here, we observed a marked induction of Id2 during cardiomyocyte differentiation from P19CL6 murine embryonic teratocarcinoma stem cells, prompting us to investigate the upstream regulatory mechanism of Id2 induction. Computer analysis of Id2 promoter and subsequent electrophoretic mobility shift assay revealed several binding sites for GATA4 and Nkx2.5 within the Id2 promoter. By further deletion and mutation analysis of the respective binding site, we identified that two motifs located at -497/-502 and -264/-270 were functionally important for Id2 promoter activation by GATA4 and Nkx2.5, respectively. Overexpression of GATA4 and/or Nkx2.5 induced not only Id2 promoter activity but also Id2 protein expression. Additionally, Id proteins significantly inhibit the GATA4 and Nkx2.5-dependent transcription, suggesting Id proteins may play a regulatory role in cardiogenesis. Collectively, our results demonstrate that GATA4 and Nkx2.5 could be one of the upstream regulators of Id2.
机译：分化/ DNA结合（Id）抑制剂可作为参与细胞谱系定型和分化的螺旋-环-螺旋蛋白的调节剂。在这里，我们观察到从P19CL6小鼠胚胎性畸胎癌干细胞分化为心肌细胞期间Id2的显着诱导，促使我们研究Id2诱导的上游调节机制。 Id2启动子的计算机分析和随后的电泳迁移率变动分析揭示了Id2启动子中GATA4和Nkx2.5的几个结合位点。通过进一步删除和相应的结合位点的突变分析，我们确定了位于-497 / -502和-264 / -270的两个基序分别对GATA4和Nkx2.5激活Id2启动子功能很重要。 GATA4和/或Nkx2.5的过度表达不仅诱导Id2启动子活性，而且诱导Id2蛋白表达。此外，Id蛋白可显着抑制GATA4和Nkx2.5依赖性转录，表明Id蛋白可能在心脏发生中起调节作用。总的来说，我们的结果表明GATA4和Nkx2.5可能是Id2的上游调节子之一。

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