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. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Trends Pharmacol Sci. 2018 Jan 28;39(2):200–208. doi: 10.1016/j.tips.2017.11.009

Figure 2.

Figure 2

Schematic contrasting current view of functional impact of localized signaling transduced by β-arrestins and Gs. Top panel: GPCR-mediated activation of β-arrestins in the PM is thought to produce a rapid ERK response that can access nuclear targets. Activation in endosomes produces delayed ERK activation and sequesters ERK in the cytoplasm, thereby preventing access to nuclear targets. Bottom panel: GPCR-mediated activation of Gs in the PM produces a rapid and transient response that activates cAMP-dependent targets in the PM and cytoplasm. Activation in endosomes produces a delayed response that preferentially accesses nuclear targets (induction of the cAMP-responsive gene PCK1 is shown as an example. For GPCRs that are capable of efficient recycling, PM and endosome-initiated activation waves can occur repeatedly in the prolonged presence of agonist through multiple rounds of endocytosis and recycling (depicted as curved arrows).