A kinase-inactive type II TGFβ receptor impairs BMP signaling in human breast cancer cells

被引:23
作者
Dumont, N
Arteaga, CL
机构
[1] Vanderbilt Univ, Sch Med, Dept Canc Biol, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Nashville, TN 37232 USA
关键词
transforming growth factor-beta; bone morphogenetic protein; dominant negative type II TGF beta receptor; signaling; MDA-MB-231;
D O I
10.1016/S0006-291X(02)02977-7
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
Dominant negative receptor mutants are often utilized in order to abrogate signaling induced by growth factors. We have previously shown that expression of a dominant negative type 11 TGFbeta receptor (dnTbetaRII) in MDA-MB-231 breast cancer cells effectively abrogates TGFbeta signaling. In this letter, we report that expression of dnTbetaRII also impairs BMP2-mediated Smad1 phosphorylation as well as BMP2-mediated Smad-dependent transcriptional responses, resulting in an attenuation of BMP-mediated anti-proliferative effects. The fact that dnTbetaRII not only abrogates TGFbeta signaling but BMP signaling as well has important implications for the interpretation of data in which dominant negative mutants are utilized. (C) 2002 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:108 / 112
页数:5
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