PathwayStep670 Effects of PIP2 hydrolysis The Ligand:GPCR:Gq complex dissociates G alpha (q) auto-inactivates by hydrolysing GTP to GDP Inactive G alpha (q) reassociates with G beta:gamma G alpha (q) inhibits PI3K alpha PLC beta-mediated PIP2 hydrolysis G alpha (q) binds to Trio family RhoGEFs PLC beta is activated by G alpha (q) GRK2 sequesters activated Gq GRK5 sequesters activated Gq Liganded Gq-activating GPCRs bind inactive heterotrimeric Gq Liganded Gq/11-activating GPCRs act as GEFs for Gq/11 PathwayStep5753 PathwayStep5755 PathwayStep5754 PathwayStep5757 PathwayStep5756 PathwayStep5759 PathwayStep5758 PathwayStep5760 PathwayStep5761 PathwayStep5762 PathwayStep5763 G alpha (q) signalling events Authored: Jupe, S, 2009-03-09 15:04:20 Edited: Jupe, S, 2009-03-09 15:04:20 Pubmed16102047 Pubmed19212139 Pubmed9296496 Reactome Database ID Release 43416476 Reactome, http://www.reactome.org ReactomeREACT_18283 Reviewed: Akkerman, JW, 2009-06-03 The classic signalling route for G alpha (q) is activation of phospholipase C beta thereby triggering phosphoinositide hydrolysis, calcium mobilization and protein kinase C activation. This provides a path to calcium-regulated kinases and phosphatases, GEFs, MAP kinase cassettes and other proteins that mediate cellular responses ranging from granule secretion, integrin activation, and aggregation in platelets. Gq participates in many other signalling events including direct interaction with RhoGEFs that stimulate RhoA activity and inhibition of PI3K. Both in vitro and in vivo, the G-protein Gq seems to be the predominant mediator of the activation of platelets.