Alroy I, Yarden Y
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
FEBS Lett. 1997 Jun 23;410(1):83-6. doi: 10.1016/s0014-5793(97)00412-2.
Ligand-induced activation of receptor tyrosine kinases (RTK) results in the initiation of diverse cellular pathways, including proliferation, differentiation and cell migration. The ErbB family of RTKs represents a model for signal diversification through the formation of homo- and heterodimeric receptor complexes. Each dimeric receptor complex will initiate a distinct signaling pathway by recruiting a different set of Src homology 2- (SH2-) containing effector proteins. Further complexity is added due to the existence of an oncogenic receptor that enhances and stabilizes dimerization but has no ligand (ErbB-2), and a receptor that can recruit novel SH-2-containing proteins, but is itself devoid of kinase activity (ErbB-3). The resulting signaling network has important implications for embryonic development and malignant transformation.
配体诱导的受体酪氨酸激酶（RTK）激活会引发多种细胞途径，包括增殖、分化和细胞迁移。RTK的表皮生长因子受体（ErbB）家族是通过形成同二聚体和异二聚体受体复合物实现信号多样化的一个模型。每个二聚体受体复合物通过招募一组不同的含Src同源2（SH2）结构域的效应蛋白来启动一条独特的信号通路。由于存在一种增强并稳定二聚化但无配体的致癌受体（ErbB-2）以及一种可招募新型含SH2结构域蛋白但其本身缺乏激酶活性的受体（ErbB-3），使得情况更加复杂。由此产生的信号网络对胚胎发育和恶性转化具有重要意义。
