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作 者:霍艳英[1] 胡迎春[1] 徐勤枝[1] 项晓琼[1] 段瑞峰[1] 李刚[1] 张开泰[1] 吴德昌[1]
机构地区:[1]军事医学科学院放射医学研究所四室,中国北京100850
出 处:《生命科学研究》2004年第3期231-236,共6页Life Science Research
基 金:国家重点基础研究发展规划973项目(G1998051207)
摘 要:Smad7是TGF-β家族信号转导通路的抑制分子,可反馈调节TGF-β/Smads信号转导通路,从功能推测,Smad7表达紊乱,可影响细胞对TGF-β的应答,从而促进细胞的恶性化进展,为了深入探讨Smad7基因功能,通过设计引物,用Touchdown巢式-PCR法从人胎脑文库中扩增Smad7基因编码区全长,回收产物,克隆并构建真核表达载体,同融合有报告基因的c-myc顺式增强子元件共转染BEP2D细胞,结果表明:TGF-β可抑制c-myc报告基因的活性,Smad7基因可正调控c-myc报告基因的表达,并拮抗TGF-β对该基因的抑制作用.由此得出结论:Smad7基因通过拮抗TGF-β来调控c-myc基因.Smad7 was identified as a TGF β inducible antagonist TGF β signaling and might participate in a negative feedback loop to control TGF β signaling. The disorder of its expression should influence cells responsiveness to TGF β and contribute to the process of cell's malignant transformation. To further investigate the gene function of Smad7, the full coding region of Smad7 was cloned and Smad7 mammalian expression vector were constructed. Transient co transfection was performed to examin the regulation of c myc by Smad7 gene. The results showed that in BEP2D cells, TGF β can inhibit the activity of c myc reporter, when co transfection with Smad7, the reporters activity increased. The results suggest that Smad7 can regulate c myc expression by antagonizing TGF β.
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