The heterotrimeric G-proteins are signaling molecules that transduce signals from a number of types of ligands such as hormones, neurotransmitters and chemokines. These extracellular signals are received by members of a large superfamily of receptors, the GPCRs, that activate the G-proteins, which then route the signals to several distinct intracellular signaling pathways. Heterotrimeric G-proteins are composed of an α, β, and γ subunit. Classically, G-proteins are divided into four families: G-αi/o, G-αs, G-αq/11, and G-α12/13, based on a similarity of their α-subunits. Each family consists of various members that often show very specific expression patterns. Members of one family are structurally similar and often share some of their functional properties. The G-αq/11 family of G proteins consists of 4 members: GNAQ, GNA11, GNA14 and GNA15/16. The α-subunits of Gq and G11 are almost ubiquitously expressed while the other members of this family such as G-α14 and G-α15/16 show a rather restricted expression pattern.The G-αq pathway transduces signals from cell surface receptors that are activated by hormones such as angiotensin-II, endothelin-1, catecholamines, and prostaglandin F2-α to regulate diverse physiological functions. The most well characterized downstream molecule of G-αq is PLC-β, the activation of which leads to the production of intracellular messengers IP3 and DAG. IP3, which accumulates rapidly and transiently, binds to IP3R in the ER and activates calcium release from the ER lumen to the cytoplasm. Calcium signaling facilitates the activation of NFATc and axonal growth. Calcium release also activates PKC-mediated Raf/MEK/ERK signaling. G-αq, working through PKC appears to regulate various isoforms of PLD. PLDs catalyze the hydrolysis of phosphatidylcholine to produce phosphatidic acid and choline, which take part in cell activation. G-αq activates the transcription factor NF-κB through PYK2. Receptors transmitting signals through G-αq can promote Rho activation. ROCK acts downstream of Rho to regulate cytoskeletal rearrangements. G-αq activates CSK which in turn phosphorylates GSK3β thus playing a role in glycogen metabolism. Negative regulators of G-αq include the RGS proteins. G-protein mediated pathways interact with one another to form a network that regulates metabolic enzymes, ion channels, transporters, and other components of the cellular machinery controlling a broad range of cellular processes, including transcription, motility, contractility, and secretion.