Ski, SnoN, and Akt as Negative Regulators of Smad Activity: Balancing Cell Death and Cell Survival

Ski, SnoN, and Akt as Negative Regulators of Smad Activity: Balancing Cell Death and Cell Survival
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Ski、SnoN 和 Akt 作为 Smad 活性的负调节因子:平衡细胞死亡和细胞存活

DOI:
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发表时间:
2008
期刊:
影响因子:
--
通讯作者:
K. Luo
K. Luo
中科院分区:
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文献类型:
--
作者:
E. L. Scolan;K. Luo

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转化生长因子-β(TGF-β)超家族的细胞因子通过募集Smad蛋白激活TGF-β靶基因的转录而发挥其多种不同的作用。Smad蛋白的活性已显示通过与细胞伴侣的相互作用来调节。其中,Ski家族的原癌基因Ski和SnoN以及蛋白激酶Akt可以通过不同的机制负性调节Smad信号传导,从而影响各种下游TGF-β反应。在这里,我们综述了Ski,SnoN和Akt如何作为Smad活性的抑制剂来拮抗TGF-β信号转导。
Cytokines of the transforming growth factor-β (TGF-β) superfamily exert many of their diverse effects via the recruitment of the Smad proteins to activate transcription of TGF-β target genes. Activities of the Smad proteins have been shown to be regulated through interaction with cellular partners. Among these, the protooncogenes of the Ski family, Ski, and SnoN, and the protein kinase Akt can negatively modulate the Smad signaling via differents mechanisms to affect various downstream TGF-β responses. Here, we review how Ski, SnoN, and Akt act as repressors of Smad activity to antagonizes TGF-β signaling.
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