Dikic I, Blaukat A
Ludwig Institute for Cancer Research, Uppsala, Sweden.
Cell Biochem Biophys. 1999;30(3):369-87. doi: 10.1007/BF02738120.
Abundant evidence has indicated that protein tyrosine kinases (PTKs) convey signals from G protein-coupled receptors (GPCRs) to regulate cell proliferation, migration, adhesion, and potentially cellular transformation. Molecular mechanisms by which PTKs regulate such diverse effects in GPCR signaling are not well understood. Recently, an unifying theme has emerged where both growth factors and GPCRs utilize protein tyrosine kinase activity and the highly conserved Ras/MAP kinase pathway to control mitogenic signals. Additionally, PTKs are also involved in the regulation of signal transmission from GPCRs to activation of the JNK/SAPK kinase pathway. Furthermore novel insights in chemokine receptor-activated PTKs and their role in mediating cell functions are discussed in this review.
大量证据表明,蛋白酪氨酸激酶(PTK)传递来自G蛋白偶联受体(GPCR)的信号,以调节细胞增殖、迁移、黏附以及潜在的细胞转化。PTK在GPCR信号传导中调节这些不同效应的分子机制尚未完全清楚。最近,出现了一个统一的观点,即生长因子和GPCR都利用蛋白酪氨酸激酶活性和高度保守的Ras/丝裂原活化蛋白激酶(MAP)途径来控制有丝分裂信号。此外,PTK还参与从GPCR到JNK/应激激活蛋白激酶(SAPK)途径激活的信号传递调节。此外,本综述还讨论了趋化因子受体激活的PTK及其在介导细胞功能中的作用的新见解。