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Biochem Biophys Res Commun. 2002 Jan 11;290(1):539-45.

Apelin (65-77) activates extracellular signal-regulated kinases via a PTX-sensitive G protein.

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  • 1Unité INSERM U-397, CHU Rangueil, Bât. L3, 1 avenue Jean-Poulhès, 31403-Toulouse, France.


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.

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