G-protein-coupled receptors (GPCRs) constitute the largest family of cell-s
urface molecules involved in signal transmission, These receptors play key
physiological roles and their dysfunction results in several diseases. Rece
ntly, it has been shown that many of the cellular responses mediated by GPC
Rs do not involve the sole stimulation of conventional second-messenger-gen
erating systems, but instead result from the functional integration of an i
ntricate network of intracellular signaling pathways. Effecters for GPCRs t
hat are independent oi G proteins have now also been identified, thus chang
ing the conventional view of the GPCR-heterotrimeric-G-protein-associated e
ffector. The emerging information is expected to help elucidate the most ba
sic mechanism by which these receptors exert their numerous physiological r
oles, in addition to determining why the perturbation of their function res
ults in many pathological conditions.