Assessing the Role of Gαq/11 in Cellular Responses: An Analysis of Investigative Tools

Seven transmembrane G Protein Coupled Receptors (GPCRs) are one of the major classes of cell surface receptors and play a major role through agonists and antagonists in human therapeutics [1]. GPCRs are associated with a group of G proteins which consist of 3 subunits termed alpha, beta and gamma. G proteins may be classified according to their effector molecules of the alpha subunit, which in mammals falls into several subtypes, Gαs, Gαi, Gα12 and Gαq. The Gαq family consists of four subunits Gαq, Gα11, Gα14 and Gα15/16. In contrast to the protein kinase receptors which have intrinsic (kinase) enzymatic activity, GPCRs do not have enzymatic activity-enzymatic activity mediating signal transduction resides in the Gα proteins which have GTPase activity [2]. Gα proteins exist in the GTP bound form. Ligand initiated conformational changes in the GPCR causes the release of bound Gα proteins. This dissociation initiates the GTPase activity, hydrolyzing GTP to GDP which is released from the proteins and allows alterative interactions leading to downstream signal transduction.