Figure 1.

Summary of G protein and arrestin-mediated signal pathways activated by FSHR. Upon ligand binding FSHR has been reported to couple to Gαs, Gαq/11, and Gαi/o heterotrimeric G proteins to mediate its downstream effects, both those in the gonads such as spermatogenesis, steroidogenesis, and follicular development, and more recently at non-gonadal sites, see text for further details. The archetypal view of GPCR signaling occurs in a G protein-dependent manner, however, agonist-activated, phosphorylated receptor recruits arrestin, for G protein signal desensitization and internalization via clathrin-coated pits. Furthermore, arrestin mediates signaling pathways independent of G proteins. This can occur through the scaffolding protein binding signaling proteins such as components of MAPK pathways after G protein activation, or independent of FSHR by complexing and activating ribosomal protein, p70S6K.