Holding their own: the noncanonical roles of Smad proteins.
Holding their own: the noncanonical roles of Smad proteins.
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DOI：
10.1126/scisignal.146pe48
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发表时间：
2008-11-18
影响因子：
7.3
通讯作者：
Kubalak SW
中科院分区：
文献类型：
--
作者：
Hoover LL;Kubalak SW
1995年Smads作为蛋白质转录因子的鉴定导致了经典转化生长因子-β（TGF-β）信号通路的阐明。在接下来的几年里，人们已经意识到了该途径的细微差别，并且现在已经理解了配体到受体到活化转录因子的简单方案在每一步都受到高度调节，并且充满了来自其他途径的串扰。Smads也被认为是典型TGF-β依赖性信号传导之外的重要参与者，并负责调节多种细胞过程。新的证据表明，Smad 7通过直接调节β-catenin在维持细胞-细胞粘附中起着不可或缺的作用。受体激活的Smads调节microRNA的一个子集的加工，特别是miR-21。证明Smads与典型TGF-β信号传导之外的蛋白质相互作用的报告数量正在增加，尽管这些相互作用的功能相关性尚不清楚。研究这些相互作用可能会产生更多的证据，表明Smads除了作为TGF-β途径中的信号转导子的原始报告功能之外，还具有重要和不同的目的。
The identification of Smads as protein transcription factors in 1995 led to elucidation of the canonical transforming growth factor–β (TGF-β) signaling pathway. In the years that have followed, nuances of the pathway have been realized, and the once-simple scheme of ligand to receptor to activated transcription factor is now understood to be highly regulated at each step and riddled with crosstalk from other pathways. The Smads are also recognized as important players outside of canonical TGF-β–dependent signaling and are responsible for regulating diverse cellular processes. New evidence suggests that Smad7 plays an integral role in maintaining cell-cell adhesion through direct regulation of β-catenin. Receptor-activated Smads regulate the processing of a subset of microRNAs, particularly miR-21. The number of reports demonstrating the interactions of Smads with proteins outside of canonical TGF-β signaling is increasing, although the functional relevance of these interactions is not known. Investigating these interactions will likely yield more evidence that Smads serve important and diverse purposes beyond their original reported function as signal transducers in the TGF-β pathway.
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DOI：
10.1091/mbc.1.11.791
发表时间：
1990-10-01
期刊：
CELL REGULATION
影响因子：
--
作者：
CHOI, Y;FUCHS, E
通讯作者：
FUCHS, E
影响因子：
5.3
作者：
Schmierer, B;Hill, CS
通讯作者：
Hill, CS
影响因子：
16
作者：
Dong, CM;Li, ZR;Goldschmidt-Clermont, PJ
通讯作者：
Goldschmidt-Clermont, PJ
影响因子：
3.7
作者：
Halder, SK;Beauchamp, RD;Datta, PK
通讯作者：
Datta, PK
影响因子：
64.8
作者：
Davis, Brandi N.;Hilyard, Aaron C.;Hata, Akiko
通讯作者：
Hata, Akiko