Gq

Gq, in a biological context, refers to the G alpha q (Gαq) subtype of heterotrimeric G proteins that participate in G protein-coupled receptor (GPCR) signaling. In humans, Gαq is encoded by the GNAQ gene and, together with predominantly GNA11, forms a subclass within the Gq/11 family that activates phospholipase C beta (PLCβ) enzymes when a GPCR is stimulated.

Mechanism and signaling, Gαq cycles between an inactive GDP-bound form and an active GTP-bound form. Upon GPCR activation, GDP is exchanged for GTP on Gαq, which then dissociates from the Gβγ dimer and activates PLCβ. PLCβ hydrolyzes PIP2 into IP3 and DAG. IP3 increases intracellular calcium, while DAG activates protein kinase C and other downstream effectors. The signal is terminated as Gαq hydrolyzes GTP to GDP, aided by regulatory proteins such as RGS proteins, and the Gαq subunit re-associates with Gβγ.

Physiological roles of Gαq signaling are diverse and include regulation of vascular smooth muscle tone, cardiac function, platelet activation, and various neuronal processes. It transduces signals from multiple GPCRs, including α1-adrenergic, angiotensin II, vasopressin, and certain muscarinic receptors, among others.

Clinical relevance: mutations in GNAQ and GNA11 are implicated in several conditions. Somatic mutations in GNAQ, especially at residues Q209 and R183, are common in uveal melanoma and in capillary malformations seen in Sturge-Weber syndrome, where constitutive PLCβ signaling drives abnormal cellular activity. These mutations are active areas of research for potential targeted therapies.