摘要目的　综述Smads蛋白结构和调节核内特异基因表达机制的最新研究成果.资料来源　MEDLINE/CD-ROM(1997-2000)和中文期刊索引（1997-2000）.研究选择　选择国内和国外新近发表的关于TGF-β超家族信号传导方面的原始文件.资料摘录　资料主要引自与本文目的密切相关的22篇文献.结果　TGF-β家族成员与细胞膜上受体结合后,通过Smads蛋白,调节细胞核内特异的基因表达.从结构和功能上看,Smads蛋白可以分为三类：受体调节-Smads (R-Smads)作为具有Ser/Thr激酶活性的受体-Ⅰ的直接底物,磷酸化后被激活,通过MH2结构域,与共同介导的Smads(Co-Smads)相互作用,形成异聚体,进入细胞核内,直接与目的基因启动子相结合,影响基因表达；而抑制转录Smads(I-Smads)能够拮抗R-Smads的生物活性.在细胞内,Smads蛋白通过与不同的转录蛋白或转录共调节因子相互作用,在不同类型的细胞内介导特异的基因表达.改变Smads蛋白的正常结构和功能能引起人体发生各种病变,如：组织纤维化、瘢痕和肿瘤发生等等.结论　Smads蛋白的结构决定其作为信使分子介导外界信号进入核内.在细胞核内,Smads蛋白能够调节TGF-β超家族依赖的基因表达.

abstractsPurpose To review the recent developments in the structure and function of Smad proteins. Data Sources Both Chinese- and English-language literatures were searched using MEDLINE/CD-ROM (1997-2000) and the Index of Chinese-Language Literature (1997-2000). Study Selection Data from published articles about TGF-β signal transduction in recent domestic and foreign literature were selected. Data Extraction Data were mainly extracted from 22 articles which are listed in the reference section of this review. Results Smad proteins mediate signal transduction induced by the TGF-β superfamily. Based on their structural and functional properties, Smad proteins are divided into three groups. The first group, receptor-regulated Smads (R-Smads), are phosphorylated by activated type Ⅰ receptors and form heteromeric complexes with the second group of Smads, common mediator Smads (Co-Smads). These Smad complexes translocate into the nucleus to influence gene transcription. Inhibitory Smads (I-Smads) are the third group and these antagonize the activity of R-Smads. In the nucleus, Smads can directly contact Smad-binding elements (SBE) in target gene promoters. Through interaction with different transcription factors, transcriptional co-activators or co-repressors, Smads elicit different effects in various cell types. The aberrance of Smad proteins has been noted in several human disorders such as fibrosis, hypertrophic scarring and cancer. Conclusion The structure of Smads determines their function as transcriptional factors which translocate signals from the cell surface to the nucleus where Smads regulate TGF-β superfamily-dependent gene expression.