Fig. 6
From: Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling
Carvedilol-induced β1AR-mediated ERK phosphorylation is dependent on both Gαi and β-arrestins. a The effect of PTX and β-arrestin knockdown on carvedilol-stimulated ERK phosphorylation. β1AR stable cells with transfection of control siRNA or β-arrestin1/2 siRNA were pretreated with vehicle or PTX, then simulated with 10 μM carvedilol for 5 min or 30 min. Carvedilol-stimulated ERK phosphorylation was diminished by either PTX pretreatment or β-arrestins siRNA, suggesting the requirement of Gαi and β-arrestins for this signaling. b The β1AR-mediated ERK phosphorylation in β-arrestin or Gαi knockout cells. Wild type, β-arrestin knockout or Gαi knockout HEK293 cells were transfected with FLAG-tagged β1ARs. Cells were stimulated with 10 μM carvedilol for 5 or 30 min, 10 μM isoproterenol or 10 ng per ml EGF for 5 min. The depletion of either β-arrestins or Gαi impaired carvedilol-induced ERK phosphorylation. Data represent the mean ± SEM for n independent experiments as marked on the figure. Statistical significance vs. unstimulated cells was assessed using one-way ANOVA with Bonferroni correction
