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首页> 外文期刊>Molecular and Cellular Biology >B-Cell Translocation Gene 2 (Btg2) Regulates Vertebral Patterning by Modulating Bone Morphogenetic Protein/Smad Signaling
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B-Cell Translocation Gene 2 (Btg2) Regulates Vertebral Patterning by Modulating Bone Morphogenetic Protein/Smad Signaling

机译：B细胞移位基因2（Btg2）通过调节骨形态发生蛋白/ Smad信号调节椎骨形态。

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Btg2 is a primary p53 transcriptional target gene which may function as a coactivator-corepressor and/or an adaptor molecule that modulates the activities of its interacting proteins. We have generated Btg2-null mice to elucidate the in vivo function of Btg2. Btg2-null mice are viable and fertile but exhibit posterior homeotic transformations of the axial vertebrae in a dose-dependent manner. Consistent with its role in vertebral patterning, Btg2 is expressed in the presomitic mesoderm, tail bud, and somites during somitogenesis. We further provide biochemical evidence that Btg2 interacts with bone morphogenetic protein (BMP)-activated Smads and enhances the transcriptional activity of BMP signaling. In view of the genetic evidence that reduced BMP signaling causes posteriorization of the vertebral pattern, we propose that the observed vertebral phenotype in Btg2-null mice is due to attenuated BMP signaling.
机译： Btg2 是一个主要的p53转录靶基因，可以作为共激活因子和/或调节其相互作用蛋白活性的衔接子分子起作用。我们已经产生了 Btg2 -null小鼠，以阐明 Btg2的体内功能。 Btg2 -null小鼠是活的和可育的，但表现出轴向椎骨的后同种异体转化，呈剂量依赖性。 Btg2 与它在椎骨形态中的作用一致，在早熟的中胚层，尾芽和体节中表达。我们还提供了生化证据，证明 Btg2 与骨形态发生蛋白（BMP）激活的Smads相互作用并增强BMP信号传导的转录活性。鉴于遗传证据表明减少BMP信号传导会导致椎骨形态的后继化，我们提出在 Btg2 -null小鼠中观察到的椎骨表型是由于BMP信号传导减弱所致。

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