Induction of Smad6 mRNA by bone morphogenetic proteins

被引：146

作者：

Takase, M

Imamura, T

Sampath, TK

Takeda, K

Ichijo, H

Miyazono, K

Kawabata, M

机构：

[1] Japanese Fdn Canc Res, Inst Canc, Dept Biochem, Toshima Ku, Tokyo 170, Japan

[2] Japan Soc Promot Sci, Japanese Fdn Canc Res, Toshima Ku, Tokyo 170, Japan

[3] Japan Soc Promot Sci, Res Future Program, Toshima Ku, Tokyo 170, Japan

[4] Creat Biomol Inc, Hopkinton, MA 01748 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 244卷 / 01期

基金：

日本科学技术振兴机构;

关键词：

D O I：

10.1006/bbrc.1998.8200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Members of the transforming growth factor-beta (TGF-beta) superfamily transduce signals via Smad proteins. Smad2 and Smad3 mediate TGF-beta signaling, whereas Smad1 and Smad5 transduce bone morphogenetic protein (BMP) signals. Smad4 is a common mediator required for both pathways. Smad6 and Smad7 are recently identified members in the Smad family; they inhibit the signaling activity of the other Smad proteins. Here we show that expression of the Smad6 mRNA is dramatically induced by BMP-2 or osteogenic protein-1 (OP-1)/BMP-7 in various cells. BMP-2 induced expression of Smad7 in one cell type, although much less potently than that of Smad6. Smad6 message was induced by TGF-beta 1 in TGF-beta 1-responsive Mv1Lu cells, but the induction was transient in contrast to the induction by BMPs. These results indicate that Smad6 may form a feedback loop to regulate the signaling activity of BMPs. (C) 1998 Academic Press.

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收藏

页码：26 / 29

页数：4

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