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首页> 外文期刊>Hepatology research: the official journal of the Japan Society of Hepatology >Involvement of Smad proteins in TGF-beta and activin A-induced apoptosis and growth inhibition of liver cells.
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Involvement of Smad proteins in TGF-beta and activin A-induced apoptosis and growth inhibition of liver cells.

机译:Smad蛋白质参与及护苯丙酸诺龙A-induced细胞凋亡和抑制增长的肝细胞。

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摘要

Transforming growth factor (TGF)-beta and activin A inhibit the growth and induce cell death of parenchymal liver cells. Smad proteins have recently been identified as intracellular signaling mediators and modulators of TGF-beta family members. This study assessed the role of Smad proteins during the action of TGF-beta and activin A on liver cells using a well-differentiated human hepatoma cell line, Hep3B cells. To study the role of Smad proteins in the anti-proliferative, apoptosis-inducing, activities of TGF-beta and activin A in liver cells, we stably transfected dominant negative Smad2-3SA or Smad3-3SA mutants in Hep3B cells. Transfection of Smad2-3SA or Smad3-3SA abrogated both TGF-beta-induced and activin A-induced growth inhibition and apoptosis of Hep3B cells. Down regulation of Bcl-xL expression by TGF-beta was both Smad2 and Smad3 dependent. We also demonstrate that transfection of Smad7, an intracellular antagonist of Smad signaling, inhibited both TGF-beta- and activin A-induced apoptosis and growth inhibition of these cells. These results suggest that Smad proteins positively and negatively mediate TGF-beta-induced and activin A-induced apoptosis and growth inhibition of liver cells.
机译:转化生长因子β(TGF)和苯丙酸诺龙抑制的生长和诱导细胞死亡肝实质细胞。最近被确认为细胞内信号介质和鉴定及调节器家庭成员。Smad蛋白质鉴定及行动中苯丙酸诺龙肝细胞上使用人类肝癌细胞系分化良好型的,Hep3B细胞。anti-proliferative,凋亡诱导,活动及和苯丙酸诺龙在肝脏细胞,我们稳定转染占主导地位的消极Smad2-3SA或Hep3B Smad3-3SA突变体的细胞。转染Smad2-3SA或Smad3-3SA废除TGF-beta-induced和苯丙酸诺龙A-inducedHep3B细胞的生长抑制和凋亡。监管及Bcl-xL表达的既Smad2 Smad3依赖。Smad7的表明转染细胞内对手Smad信号,抑制及和苯丙酸诺龙A-induced这些细胞的凋亡和抑制增长。这些结果表明,Smad蛋白质积极的和消极的调解TGF-beta-induced和苯丙酸诺龙A-induced细胞凋亡和肝细胞生长抑制。

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