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TGF-β1/Smad3信号途径对牙本质涎磷蛋白基因表达的调控 被引量:3

Regulating function of TGF-β1/Smad3 to dentin sialophosphoprotein gene promoter
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摘要 目的:研究小鼠成牙本质细胞系MDPC-23中TGF-β1及其信号分子Smad3对小鼠牙本质涎磷蛋白(dentin sialophosphoprotein,DSPP)基因表达中的调控作用。方法:PCR法制备DSPP引物、构建带有DSPP启动子片段的萤火虫荧光素酶基因报告载体,通过瞬时转染入MDPC-23细胞后,检测报告基因活性。结果:在TGF-β1的作用下,Smad3可以发生转位表达,由细胞浆转入细胞核内。同时,过表达野生型Smad3可以显著增强TGF-β1对DSPP启动子活性的下调作用。结论:TGF-β1可以通过Smad3信号通路对DSPP启动子进行调控;在DSPP启动子-2525^+54bp之间,存在TGF-β1/Smad3信号途径的结合位点,从而发挥对DSPP基因的调控作用。 Objective: To characterize the role of TGF-β1/Smad3 proteins in transcriptional regulation of dentin sialophosphoprotein (DSPP) in mouse odontoblast cell line MDPC-23. Methods: PCR, construct luciferase reporter gene vectors, transient transfection and luciferase assay were used. Results: Transforming growth factor- β1 (TGF- β1) could induce Smad3 transposition from cytoplasm to nucleus, and wild type Smad3 could strengthen the TGF-β1 inhibitory action to DSPP. Conclusion: TGF-β1/Smad3 signal can regulate DSPP promoter segments. There are TGF-β1s starting element in the region -2525 - +54bp of DSPP promoter.
出处 《中华老年口腔医学杂志》 2008年第3期155-158,182,共5页 Chinese Journal of Geriatric Dentistry
基金 国家自然科学基金资助项目(30200315)
关键词 牙本质涎磷蛋白 启动子 报告基因 SMAD3 TGF-Β1 dentin sialophosphoprotein promoter reporter gene Smad3 TGF-β1
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