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Keywords: arrestin
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Biochem Soc Trans (2013) 41 (1): 137–143.
Published: 29 January 2013
... degrade extracellular neuropeptides, and receptor interaction with β-arrestins, which uncouple receptors from heterotrimeric G-proteins and mediate receptor endocytosis. By recruiting GPCRs, kinases and phosphatases to endocytosed GPCRs, β-arrestins assemble signalosomes that can mediate a second wave of...
Biochem Soc Trans (2013) 41 (1): 144–147.
Published: 29 January 2013
.... Importantly, distinct effector proteins (G-proteins and arrestins) as well as ligands are likely to affect the conformational landscape of GPCRs in different manners, as we show with the isolated ghrelin receptor. Such modulation of the GPCR conformational landscape by pharmacologically distinct ligands and...
Biochem Soc Trans (2013) 41 (1): 218–224.
Published: 29 January 2013
... arrestin biased agonism efficacy GPCR G protein μ-opioid receptor Classical ideas of GPCR (G-protein-coupled receptor) function describe drug action in terms of affinity and efficacy, where affinity reflects the tendency of the drug to interact with the receptor whereas efficacy describes the...
Biochem Soc Trans (2004) 32 (6): 1029–1031.
Published: 26 October 2004
... energy transfer to quantify the kinetics of receptor activation by agonist (measured as conformational change in the receptor), the kinetics of G-protein activation (measured as G-protein subunit rearrangement) and the kinetics of receptor inactivation by arrestins (measured as receptor–arrestin...
Biochem Soc Trans (2003) 31 (6): 1186–1190.
Published: 01 December 2003
... elevated cAMP levels cause PKA (protein kinase A) to phosphorylate UCR1 and ablate the inhibitory action of ERK. PDE4 isoforms can also be found in complex with β-arrestins where they provide a novel part of the cellular desensitization mechanism to receptor-mediated cAMP signalling. Stimulation of the β 2...