| 1 | Regulation of TGF-β signaling by Smad7显示文摘转变生长因素(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。 | Xiaohua Yan Ziying Liu Yeguang Chen | 2009 | Acta Biochimica et Biophysica Sinica2009，41，4： | 42 |
| 2 | Yin Yang 1(YY1) synergizes with Smad7 to inhibit TGF-β signaling in the nucleus显示文摘As a prototype of the TGF-βsuperfamily cytokines,TGF-βis well known for its diverse roles in embryogenesis and adult tissue homeostasis.TGF-βevokes cellular responses by signaling mainly through cell membrane receptors and transcription factor R-Smads and Co-Smad(Smad4),while an inhibitory Smad,Smad7,acts as a critical negative regulator of TGF-βsignaling.Smad7 antagonizes TGF-βsignaling by regulating the stability or activity of the receptors or blocking the DNA binding of the functional R-Smad-Smad4 complex in the nucleus.However,the function of Smad7 in the nucleus is not fully understood.Yin Yang 1(YY1)is a ubiquitously expressed transcription factor with multiple functions.It has been reported that YY1 can inhibit Smad-dependent transcriptional responses and TGF-β/BMP-induced cell differentiation independently of its DNA binding ability.In this study,we found that Smad7 interacts with YY1 and the interaction is attenuated by TGF-βsignaling.Reporter assays and target gene expression analyses revealed that Smad7 and YY1 act in concert to inhibit TGF-β-induced transcription in the nucleus.Furthermore,Smad7 could enhance the interaction of YY1 with the histone deacetylase HDAC1.Consistently,YY1 and HDAC1 augmented the transcription repression activity of Smad7 in Gal4-luciferase reporter analysis.Therefore,our findings define a novel mechanism of Smad7 and YY1 to antagonize TGF-βsignaling. | YAN XiaoHua PAN Jun XIONG WanWan CHENG MinZhang SUN YingYuan ZHANG SuPing CHEN YeGuang | 2014 | Science China(Life Sciences)2014，57，1： | 10 |
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