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骨形态发生蛋白 (BMPs)作用于靶细胞膜上具有丝 /苏氨酸蛋白激酶活性的 Ⅱ 型受体 ,活化的 Ⅱ 型受体磷酸化Ⅰ 型受体 ,并进一步将信号传递到Smad途径。磷酸化的受体调节型Smad(R Smad)从膜受体上脱离 ,结合共同型Smad(C Smad)后 ,进入细胞核。Smad异聚体复合物在其他DNA结合蛋白的参与下作用于特异的靶基因 ,起转录调节作用。在BMPs信号传递途径中 ,存在细胞外拮抗剂、膜受体、细胞浆微环境和转录水平四个层次的调节控制。
Bone morphogenetic proteins (BMPs) act on type II receptors with filament / threonine protein kinase activity on target cell membranes, and activated type II receptors phosphorylate type I receptors and further transmit signals to the Smad pathway. The phosphorylated receptor-regulated Smad (R Smad) is released from the membrane receptor and binds to the common Smad (C Smad) and enters the nucleus. The Smad heteromeric complex acts on specific target genes with the involvement of other DNA-binding proteins and plays a transcriptional regulatory role. In the BMPs signaling pathway, there are four levels of regulation of extracellular antagonists, membrane receptors, cytoplasmic microenvironment and transcriptional level.