Wetzker Reinhard, Böhmer Frank-D
Institute for Molecular Cell Biology, Jena University Hospital, Drackendorfer Strasse 1, D-07747 JENA, Germany.
Nat Rev Mol Cell Biol. 2003 Aug;4(8):651-7. doi: 10.1038/nrm1173.
Many agonists of G-protein-coupled receptors (GPCRs) can stimulate receptor tyrosine kinases and the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway. A 'transactivation' mechanism, which links these events in one signalling chain, inspired many researchers, but inevitably raised new questions. A 'multi-track' model for GPCR signalling to the ERK/MAPK pathway might resolve some of the puzzles in the transactivation field.
许多G蛋白偶联受体（GPCRs）的激动剂能够刺激受体酪氨酸激酶以及细胞外信号调节激酶（ERK）/丝裂原活化蛋白激酶（MAPK）信号通路。一种将这些事件连接在一条信号链中的“转活化”机制启发了许多研究人员，但不可避免地也引发了新问题。一种关于GPCR向ERK/MAPK信号通路进行信号传导的“多途径”模型或许能够解决转活化领域中的一些谜题。
