When a G protein-coupled receptor does not couple to a G protein.
Classically, G protein-coupled receptors (GPCRs) relay signals by directly activating heterotrimeric guanine nucleotide-binding proteins (G proteins). Increasing evidence indicates that GPCRs may also signal through G protein-independent pathways. JAK/STATs, Src-family tyrosine kinases, GRKs/beta-arrestins, and PDZ domain-containing proteins have been suggested to directly relay signals from GPCRs independent of G proteins. In addition, our laboratory recently reported that the beta(2) adrenergic receptor (beta(2)AR) could switch from G protein-coupled to G protein-independent ERK (extracellular signal-regulated kinase) activation in an agonist dosage-dependent manner. This finding provides a novel mechanism for G protein-independent GPCR signaling. This review focuses on recent progress in understanding the mechanisms by which G protein-independent GPCR signaling occurs.
Sun
Yutong
Y
Department of Physiology, Cornell University Weill Medical College, 1300 York Ave, New York, NY 10021, USA.
McGarrigle
Deirdre
D
Huang
Xin-Yun
XY
D019204:GTP-Binding Proteins / Q000378:metabolism*; D008954:Models, Biological; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D043562:Receptors, G-Protein-Coupled; D019204:GTP-Binding Proteins