Apelin (65-77) activates extracellular signal-regulated kinases via a PTX-sensitive G protein. |
| |
Authors: | Bernard Masri Hicham Lahlou Honoré Mazarguil Bernard Knibiehler Yves Audigier |
| |
Institution: | Unité INSERM U-397, CHU Rangueil, Bat. L3, 1 avenue Jean-Poulhès, 31403-Toulouse, France. |
| |
Abstract: | We report here that apelin (65-77) induces activation of extracellular-regulated kinases (ERKs) in Chinese hamster ovary (CHO) cells expressing the msr/apj receptor. This concentration-dependent activation was transient, peaking at 5 min. Pretreatment of CHO cells with pertussis toxin fully abrogated ERK phosphorylation, whereas overexpression of the beta-adrenergic receptor kinase-1 C-terminal fragment did not alter ERK activation. Transfection with a dominant-negative mutant of Ras was without effect on ERK activation, whereas an inhibitor of many protein kinase C isoforms, GF109203X, strongly decreased it. These results demonstrate that stimulation of the murine msr/apj receptor promotes ERK activation via the alpha subunit of a pertussis toxin-sensitive protein in a Ras-independent pathway. |
| |
Keywords: | G protein-coupled receptors phosphorylation cascades endothelium vertebrate mouse |
本文献已被 ScienceDirect 等数据库收录! |
|