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首页> 外文期刊>Journal of Cellular Physiology >Transcriptional activation by stimulating protein 1 and post-transcriptional repression by muscle-specific microRNAs of IKs-encoding genes and potential implications in regional heterogeneity of their expressions.
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Transcriptional activation by stimulating protein 1 and post-transcriptional repression by muscle-specific microRNAs of IKs-encoding genes and potential implications in regional heterogeneity of their expressions.

机译：通过刺激蛋白质的转录激活1和转录后镇压IKs-encoding基因的阳性小分子核糖核酸在地区和潜在的影响异质性的表达式。

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摘要

In cardiac cells, KCNQ1 assembles with KCNE1 and forms a channel complex constituting the slow delayed rectifier current I(Ks). Expression of KCNQ1 and KCNE1 are regionally heterogeneous and changes with pathological states of the heart. The aims of this study were to decipher the molecular mechanisms for transcriptional and post-transcriptional regulation expression of KCNQ1 and KCNE1 genes and to shed light on the molecular mechanisms for their spatial heterogeneity of distribution. We cloned the 5'-flanking region and identified the transcription start sites of the KCNQ1 gene. We characterized the core promoters of KCNQ1 and KCNE1 and revealed the stimulating protein (Sp1) as a common transactivator of KCNQ1 and KCNE1 by interacting with the Sp1 cis-acting elements in the core promoter regions of these genes. We also characterized the 3' untranslated regions (3'UTRs) of the genes and experimentally established KCNQ1 and KCNE1 as targets for repression by the muscle-specific microRNAs miR-133 and miR-1, respectively. We demonstrated spatial heterogeneity of KCNQ1 and KCNE1 distributions at three axes (interventricular, transmural and apical-basal) and disparity between mRNA and protein expressions of these genes. We also found characteristic regional differences of expressions of Sp1 and miR-1/miR-133 in the heart. Our study unraveled a novel aspect of the cellular function of miRNAs and suggests that the I(Ks)-encoding genes KCNQ1 and KCNE1 expressions are dynamically balanced by transcription factor regulation and miRNA repression. The heterogeneities of Sp1 and miR-1/miR-133 offer an explanation for the well-recognized regional differences and disparity between mRNA and protein expressions of KCNQ1 and KCNE1.
机译：在心肌细胞中,KCNQ1和KCNE1和组装形成一个通道复杂构成缓慢我延迟整流电流(Ks)。KCNQ1和KCNE1异构和区域改变与心脏的病理状态。本研究的目的是解释转录和分子机制转录后调控的表达KCNQ1和KCNE1基因并阐明空间的分子机制分布的异质性。5 '侧翼区域和确定了转录KCNQ1开始网站。核心启动子的KCNQ1和特点KCNE1和揭示了刺激蛋白(Sp1)作为一种常见的KCNQ1和KCNE1反式激活因子与Sp1 cis-acting交互元素这些基因的启动子区域核心。3 '非翻译区特征(3 'utrs)的基因和实验建立KCNQ1和KCNE1作为目标阳性小分子核糖核酸的镇压mir - 133和miR-1分别。空间异质性的KCNQ1和KCNE1分布在三个轴(心室,透壁的apical-basal)和差异之间的信使rna和蛋白质的表达基因。表达式的Sp1和差异miR-1 / mir - 133心脏。小说方面的microrna的细胞功能我表明(Ks) KCNQ1基因编码和KCNE1表情动态平衡转录因子调控和microrna镇压。miR-1 / mir - 133提供了一个解释公认地区差异,差距mRNA和蛋白的表达

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