A kinase-inactive type II TGFβ receptor impairs BMP signaling in human breast cancer cells
A kinase-inactive type II TGFβ receptor impairs BMP signaling in human breast cancer cells
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DOI：
10.1016/s0006-291x(02)02977-7
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发表时间：
2003-01-31
影响因子：
3.1
通讯作者：
Arteaga, CL
中科院分区：
文献类型：
--
作者：
Dumont, N;Arteaga, CL
显性负性受体突变常被用来阻断生长因子诱导的信号转导。我们之前已经证明，在MDA-MB-231乳腺癌细胞中表达主导的负性11型TGFbeta受体(DnTbetaRII)有效地取消了TGFbeta信号。在这封信中，我们报告了dnTbetaRII的表达也损害了BMP2介导的Smad1的磷酸化以及BMP2介导的Smad依赖的转录反应，导致BMP介导的抗增殖作用的减弱。DnTbetaRII不仅取消了TGFbeta信号，也取消了BMP信号，这一事实对于解释使用显性负突变的数据具有重要意义。(C)2002年埃尔塞维尔科学公司(美国)。版权所有。
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.