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MDPC-23细胞内核心结合因子A1增强Smad3调控牙本质涎磷蛋白基因的表达

CBFA1 enhances transcriptional activation of dentin sialophosphoprotein by Smad3 in MDPC-23 cells
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摘要 目的 :研究转录因子核心结合因子A1(CBFA1)在Smad分子调控牙本质涎磷蛋白 (DSPP)基因表达中的作用。方法 :细胞培养 ,基因转染和报告基因检测。结果 :转化生长因子 β1(TGF β1)抑制DSPP基因启动子活性的表达。Smad3过表达显著增强了TGF β1对DSPP基因表达的转录抑制。单独过表达CBFA1对DSPP基因启动子活性无明显影响。但是 ,CBFA1与Smad3共转染显著增强Smad3对DSPP基因启动子的抑制作用 ,在TGF β1存在时 ,其作用进一步增强。结论 :在成牙本质细胞系MDPC 2 3内 ,CBFA1可能作为一种转录因子协同调控Smad3对DSPP基因转录的调控。 Objective:To characterize the role of core binding factor A1 (CBFA1) in transcriptional activation of dentin sialophosphoprotein (DSPP) mediated by Smad proteins.Method:Cell culture, transient transfection and luciferase assay.Result: Transforming growth factor-β 1 (TGF-β 1) inhibited the activity of DSPP promoter luciferase reporter construct containing the sequence between -1447 bp and +54 bp of mouse DSPP gene. Overexpression of wild-type Smad3 potentiated the inhibitory effect of TGF-β 1 on transcriptional regulation of DSPP gene. CBFA1 overexpression alone had no effect on the basal luciferase activity of DSPP gene promoter. However, CBFA1, combined with Smad3, significantly enhanced the transcriptional inhibitory activity of Smad3, which was further potentiated by TGF-β 1.Conclusion:These results suggest that CBFA1 maybe cooperate with Smad3 to inhibit transcription of DSPP.
出处 《临床口腔医学杂志》 2004年第12期723-725,共3页 Journal of Clinical Stomatology
基金 国家自然科学基金资助项目 (30 2 0 0 31 5)
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