Masri Bernard, Lahlou Hicham, Mazarguil Honoré, Knibiehler Bernard, Audigier Yves
Unité INSERM U-397, CHU Rangueil, Bât. L3, 1 avenue Jean-Poulhès, 31403-Toulouse, France.
Biochem Biophys Res Commun. 2002 Jan 11;290(1):539-45. doi: 10.1006/bbrc.2001.6230.
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.
我们在此报告，apelin（65 - 77）在表达msr/apj受体的中国仓鼠卵巢（CHO）细胞中诱导细胞外调节激酶（ERK）激活。这种浓度依赖性激活是短暂的，在5分钟时达到峰值。用百日咳毒素预处理CHO细胞可完全消除ERK磷酸化，而β-肾上腺素能受体激酶-1 C末端片段的过表达并未改变ERK激活。用Ras的显性负性突变体转染对ERK激活没有影响，而许多蛋白激酶C亚型的抑制剂GF109203X则强烈降低了ERK激活。这些结果表明，刺激小鼠msr/apj受体通过百日咳毒素敏感蛋白的α亚基在不依赖Ras的途径中促进ERK激活。
