Figure 3.

FSH-induced β-arrestin-dependent signaling. Initially, the perception of β-arrestins’ role was restricted to the control of FSHR’s desensitization and recycling. This view has progressively evolved toward a more general role of β-arrestins as adapters and transducers leading to the activation of MAPK ERK and rpS6 independently of G proteins upon FSH stimulation. GRK2/3 and GRK5/6 control the fate of the activated FSHR (i.e., desensitization vs. signaling) presumably through phosphorylation of distinct serines and threonines within the receptor’s C-tail.