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. Author manuscript; available in PMC: 2016 Jun 6.
Published in final edited form as: Biochem Cell Biol. 2014 Aug 20;92(6):431–440. doi: 10.1139/bcb-2014-0072

Figure 1.

Figure 1

Canonical Gα-mediated signalling at GPCRs typically following ligand binding and activation. The heterotrimeric (i.e., αβγ trimer) G-protein coupling preference and downstream cellular effect of a GPCR is defined by the Gα subunit (Gαs, Gαi/o, Gαq/11, and Gα12/13). Gαs stimulates adenylyl cyclase, producing cAMP and inducing PKA (protein kinase A) activation; Gαi/o inhibits adenylyl cyclase activity; Gαq/11 activates PLCβ, producing DAG (diacyl glycerol) and Ins(1,4,5)P3 (inositol 1,4,5-triphosphate), causing an increase in intracellular [Ca2+] and PKC activation; and, Gα12/13 activates RhoGEF, causing activation of RhoA. Arrowheads indicate activation and blunted arrows indicate inhibition. (Colour available online.)