Robert J. Lefkowitz

TL;DR: Results suggest that at steady state partial agonists transform a smaller portion of the receptor pool into the conformationally altered or activated form which serves as the substrate for beta AR kinase, although they do not completely rule out the possibility that a partial conformational change is occurring.

TL;DR: Stimulation of responsive cells by such hormones as epinephrine and other catecholamines, adrenocorticotrophic hormone, glucagon, luteinizing hormone, vasopressin, prostaglandins, and thyroid-stimulating hormone leads to increased concentrations of cAMP within the cells, leading to hormone-induced refractoriness.

TL;DR: Biased signaling and other recently appreciated complexities of GPCR signaling thus appear to be a natural consequence of the conformational heterogeneity of G protein-coupled receptors and G PCR-transducer complexes.

TL;DR: The maturation of rat reticulocytes to erythrocytes is paralleled by a marked loss of adenylate cyclase responsiveness to catecholamines and guanine nucleotides without significant loss of basal enzyme activity, which suggests that one molecular concomitant of rat ERYthrocyte maturation is a decrease in the effectiveness of receptor-guanineucleotide regulatory protein communication.

TL;DR: In studies of the mouse heart, Zhai et al. compare the physiologic and biochemical consequences of transgenic cardiac-specific overexpression of a mutant AT1R incapable of G protein coupling with those of a wild-type receptor and provide important and previously unappreciated clues as to the underlying molecular mechanisms.