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作 者:温见燕[1] 阴彬[2] 张英姿[3] 叶建伟[2] 廖文强[1] 于长安[1] 柯元南[1]
机构地区:[1]中日友好医院全国中西医结合心血管病中心,北京100029 [2]中国医学科学院基础医学研究所北京协和医学院医学分子生物学国家重点实验室,北京100005 [3]山东省泰山医学院附属医院,山东泰安271000
出 处:《基础医学与临床》2009年第4期342-346,共5页Basic and Clinical Medicine
基 金:国家自然科学基金(30700323)
摘 要:目的研究MEF2C对DOK5的表达调控机制。方法用RT-PCR法检测小鼠中DOK5组织表达谱,检测P19CL6向心肌细胞分化过程中DOK5和MEF2C的表达。MEF2C与DOK5启动子报告基因共转染P19CL6细胞或将DOK5启动子上的MEF2结合位点突变后,观察报告基因活性的变化。结果DOK5在小鼠的脑、心脏、骨骼肌等高表达。DOK5和MEF2C在P19CL6向心肌细胞分化过程中mRNA表达水平升高(P<0.05)。过表达MEF2C可以激活DOK5启动子区的报告基因活性,而MEF2结合位点突变则抑制DOK5启动子区报告基因活性。结论MEF2C可以通过作用于DOK5启动子区的MEF2结合位点,调节DOK5的转录活性。Objective To explore the effects of myocyte enhancer factor 2C (MEF2C) on the expression regulation of DOK5. Methods RT-PCR was carried out to detect the tissue distribution of mouse DOK5gene and the expression level of DOK5 and MEF2C during P19CL6 cells differentiated into cardiomyocytes. The effect of MEF2C on DOK5 promoter was confirmed by co-transfection studies. Results The expression of DOK5 was rich in brain, muscle and heart. The mRNA level of DOK5 and MEF2C was enhanced during P19CL6 cells differentiation into cardiotnyocytes ( P 〈 0. 05 ). Over-expression of MEF2C increased the promoter activity of DOK5. Furthermore, site-directed mutagenesis demonstrated that MEF2C was crucial for activating DOK5 promoter. Conclusion MEF2C enhanced the transcription of DOK5 through MEF2 binding site on DOK5 promoter.
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