作者: Hui Miao , Bih-Rong Wei , Donna M. Peehl , Qing Li , Terry Alexandrou
DOI: 10.1038/35074604
关键词: Receptor tyrosine kinase 、 MAPK/ERK pathway 、 Ephrin 、 Cell biology 、 EPH receptor A3 、 Platelet-derived growth factor receptor 、 EPH receptor B2 、 Erythropoietin-producing hepatocellular (Eph) receptor 、 Chemistry 、 EPH receptor A2
摘要: Interactions between Eph receptor tyrosine kinases (RTKs) and membrane-anchored ephrin ligands critically regulate axon pathfinding development of the cardiovascular system, as well migration neural cells. Similar to other RTKs, ligand-activated recruit multiple signalling adaptor proteins, several which are involved in growth regulation. However, contrast activation receptors fails promote cell proliferation or transform rodent fibroblasts, indicating that may initiate pathways distinct from those transmitted by RTKs. Here we show stimulation endogenous EphA with ephrin-A1 potently inhibits Ras/MAPK cascade a range types, attenuates mitogen-activated protein kinase (MAPK) for platelet-derived factor (PDGF), epidermal (EGF) vascular endothelial (VEGF). In prostatic epithelial cells cells, but not treatment proliferation. Our results identify negative regulators pathway exert anti-mitogenic functions cell-type-specific manner.