Smad-dependent and Smad-independent pathways in TGF-β family signalling

被引：4582

作者：

Derynck, R ^{[1
]}

Zhang, YE

机构：

[1] Univ Calif San Francisco, Dept Growth & Dev, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Cell Biol Program, San Francisco, CA 94143 USA

[4] Univ Calif San Francisco, Program Dev Biol, San Francisco, CA 94143 USA

[5] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA

来源：

NATURE | 2003年 / 425卷 / 6958期

关键词：

D O I：

10.1038/nature02006

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Transforming growth factor-beta (TGF-beta) proteins regulate cell function, and have key roles in development and carcinogenesis. The intracellular effectors of TGF-beta signalling, the Smad proteins, are activated by receptors and translocate into the nucleus, where they regulate transcription. Although this pathway is inherently simple, combinatorial interactions in the heteromeric receptor and Smad complexes, receptor-interacting and Smad-interacting proteins, and cooperation with sequence-specific transcription factors allow substantial versatility and diversification of TGF-beta family responses. Other signalling pathways further regulate Smad activation and function. In addition, TGF-beta receptors activate Smad-independent pathways that not only regulate Smad signalling, but also allow Smad-independent TGF-beta responses.

引用

页码：577 / 584

页数：8

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