中文摘要：

转变生长因素(TGF )- 是调整象细胞生长，区别， apoptosis，移植，细胞粘附，和免疫者那样的许多细胞的过程的多种的 cytokine 反应。在表明小径的听说得好的古典 TGF- ， TGF- 激活经由它象 TRII 和 ALK5/TRI 那样的二房间表面受体发信号的 Smad，导致调停 Smad 的 transcriptional 规定。另外， TGF- 可以也激活象激活 mitogen 的蛋白质 kinase 一样的另外的发信号的小径， PI3K，等等。发信号 TGF- 细微地在不同层次被调整。包括 Smad6 和 Smad7，禁止的 Smads 是由否定反馈环发信号的 TGF-/bone 形态基因的蛋白质(BMP ) 的关键管理者。他们能与激活的类型形成稳定的建筑群我受体并且从而堵住 R-Smads，或成员 ubiquitin E3 ligases 的 phosphorylation 例如 Smurf1/2，导致激活的类型的 ubiquitination 和降级我受体。而且，这些禁止的 Smad 蛋白质也禁止由与 transcriptional 抑压者交往，或破坏 TGF 的形成在原子核发信号的 TGF-/BMP，例如 histone deacetylases， Hoxc-8，和 CtBP -- 导致的功能的 Smad-DNA 建筑群。Smad7 被不同刺激接着调整，包括 TGF- ， IFN- ， TNF- 象一样紫外并且 TPA，并且调停在 TGF- 之间的串音和另外的发信号的小径。Smad7 表示的解除管制与各种各样的人的疾病被联系了，例如织物纤维变性，煽动性的疾病以及 carcinogenesis。Smad7 的 Overexpression 被显示了反对 TGF -- 调停的纤维变性， carcinogenesis，和发炎，建议 Smad7 的一个治疗学的潜力治疗这些疾病。

英文摘要：

Transforming growth factor （TGF）-β is a pleiotropic cytokine regulating a variety of cellular processes such as cell growth, differentiation, apoptosis, migration, cell adhesion, and immune response. In the well-understood classical TGF-β signaling pathway, TGF-β activates Smad signalling via its two cell surface receptors such as TβRII and ALK5/TβRI, leading to Smad-mediated transcriptional regulation. In addition, TGF-β may also activate other signaling pathways like mitogen-activated protein kinase, PI3K, etc. The signaling of TGF-β is finely regulated at different levels. Inhibitory Smads, including Smad6 and Smad7, are key regulators of TGF-β/bone morphogenetic protein （BMP） signaling by negative feedback loops. They can form stable complexes with activated type I receptors and thereby blocking the phosphorylation of R-Smads, or recruit ubiquitin E3 ligases, such as Smurfl/2, resulting in the ubiquitination and degradation of the activated type I receptors. Besides, these inhibitory Smad proteins also inhibit TGF-β/BMP signaling in the nucleus by interacting with transcriptional repressors, such as histone deacetylases, Hoxc-8, and CtBP, or disrupting the formation of the TGF-β-induced functional Smad-DNA complexes. Smad7 is in turn regulated by different stimuli, including TGF-[~, IFN-ff, TNF-oL as well as ultraviolet and TPA, and mediates the crosstalk between TGF-β and other signaling pathways. Deregulation of Smad7 expression has been associated with various human diseases, such as tissue fibrosis, inflammatory disease as well as carcinogenesis. Overexpression of Smad7 has been shown to antagonize TGF-β-mediated fibrosis, carcinogenesis, and inflammation, suggesting a therapeutic potential of Smad7 to treat these diseases.