2002年12月
Two major Smad pathways in TGF-beta superfamily signalling
GENES TO CELLS
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- 巻
- 7
- 号
- 12
- 開始ページ
- 1191
- 終了ページ
- 1204
- 記述言語
- 英語
- 掲載種別
- 記事・総説・解説・論説等(学術雑誌)
- 出版者・発行元
- BLACKWELL PUBLISHING LTD
Members of the transforming growth factor-beta (TGF-beta) superfamily bind to two different serine/threonine kinase receptors, i.e. type I and type II receptors. Upon ligand binding, type I receptors specifically activate intracellular Smad proteins. R-Smads are direct substrates of type I receptors; Smads 2 and 3 are specifically activated by activin/nodal and TGF-beta type I receptors, whereas Smads 1, 5 and 8 are activated by BMP type I receptors. Nearly 30 proteins have been identified as members of the TGF-beta superfamily in mammals, and can be classified based on whether they activate activin/TGF-beta-specific R-Smads (AR-Smads) or BMP-specific R-Smads (BR-Smads). R-Smads form complexes with Co-Smads and translocate into the nucleus, where they regulate the transcription of target genes. AR-Smads bind to various proteins, including transcription factors and transcriptional co-activators or co-repressors, whereas BR-Smads interact with other proteins less efficiently than AR-Smads. Id proteins are induced by BR-Smads, and play important roles in exhibiting some biological effects of BMPs. Understanding the mechanisms of TGF-beta superfamily signalling is thus important for the development of new ways to treat various clinical diseases in which TGF-beta superfamily signalling is involved.
- リンク情報
- ID情報
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- ISSN : 1356-9597
- Web of Science ID : WOS:000179797800001