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首页> 外文期刊>Journal of Cellular Physiology >Cloning and expression of a rat Smad1: regulation by TGFbeta and modulation by the Ras/MEK pathway.
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Cloning and expression of a rat Smad1: regulation by TGFbeta and modulation by the Ras/MEK pathway.

机译：一只老鼠的克隆、表达Smad1:监管通过TGFbeta和调制Ras / MEK通路。

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摘要

A new family of signaling intermediates for TGFbeta superfamily members and other growth factors has recently been identified and termed Smads. It has been suggested that the Smad1 subfamily is regulated primarily by the TGFbeta superfamily member bone morphogenetic protein (BMP). Here we demonstrate that TGFbeta induced phosphorylation of endogenous Smad1 in untransformed IECs and that the RI and RII TGFbeta receptors were detectable in Smad1 immunocomplexes. Expression of a dominant-negative mutant of Ras inhibited the ability of TGFbeta to phosphorylate endogenous Smad1. In a separate series of experiments, we have cloned a rat homologue of the drosophila mad gene (termed RSmad1) by screening an intestinal epithelial cell (IEC) cDNA library. By using an in vitro kinase assay with RSmad1 as the substrate, we demonstrate that the TGFbeta receptor complex can directly phosphorylate RSmad1. We show, further, that a dominant-negative mutant of MEK1 inhibited the ability of RSmad1 to induce the TGFbeta-responsive reporter p3TP-Lux in a human breast cancer cell line. Collectively, our data demonstrate that TGFbeta can regulate Smadl and that the Ras and MEK signaling components are partially required for the ability of TGFbeta to regulate Smad1.
机译：信号中间体的新家庭TGFbeta总科成员和其他增长最近被识别并称为因素Smads。亚科主要由TGFbeta监管总科成员骨形态形成蛋白(BMP)。内源性Smad1磷酸化untransformed iec国际扶轮和RII在Smad1 TGFbeta受体检测immunocomplexes。显性负突变的Ras抑制了TGFbeta使磷酸化内生的能力Smad1。克隆了一只老鼠同系物的果蝇疯了吗通过检查一个肠道基因(称为RSmad1)上皮细胞(IEC) cDNA图书馆。体外激酶与RSmad1作为试验衬底,我们证明TGFbeta受体复杂可以直接使磷酸化RSmad1。显性负突变MEK1抑制了RSmad1的诱导能力TGFbeta-responsive记者p3TP-Lux人类乳腺癌细胞系。证明TGFbeta可以调节Smadl和Ras和MEK信号组件部分所需TGFbeta的能力调节Smad1。

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