June 20, 2017Open Access

Genetic evidence that β-arrestins are dispensable for the initiation of β 2 -adrenergic receptor signaling to ERK

Structured PICO

Does genetic deletion of β-arrestins prevent β2AR-mediated ERK activation in cell models?

P

Population

HEK293 cells, mouse embryonic fibroblasts (MEFs) derived from Gnas f/f mice, and Rasless MEFs

I

Intervention

Genetic deletion or knockdown of β-arrestin 1 and 2, Gαs, and other signaling components, followed by stimulation with β2AR agonists (isoproterenol, epinephrine)

C

Comparator

Parental/wild-type cell lines or control siRNA/adenovirus

O

Outcome

β2AR internalization and ERK activationsurrogate

The study provides genetic evidence that β-arrestins are dispensable for β2AR-mediated ERK activation, which instead relies on Gαs and Gβγ signaling.

Abstract

AR signaling through β-arrestin-independent pathways in key physiological functions and under pathological conditions.

Genetic evidence that β-arrestins are dispensable for the initiation of β 2 -adrenergic receptor signaling to ERK

Structured PICO

Abstract

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