September 2022 "G protein-coupled receptor (GPCR) kinases (GRKs) and arrestins mediate GPCR desensitization The spatial pattern of GPCR phosphorylation is predicted to trigger these discrete GRK and arrestin-mediated We demonstrate by pharmacologic inhibition of GRK2/3-mediated phosphorylation of the chemokine receptor In conclusion, this study provides evidence that distal C-tail phosphorylation sites specify GRK-βarrestin-mediated

August 2022 "Emerging evidence suggests that G protein-coupled receptor (GPCR) kinases (GRKs) are associated However, GRKs have not been directly implicated in regulation of the amyloid-β (Aβ) pathogenic cascade Here, we determine that GRKs phosphorylate a non-canonical substrate, anterior pharynx-defective 1A ( Significantly, we show that GRKs generate distinct phosphorylation barcodes in intracellular loop 2 (

Employing GRK knockout cells and β-arrestins lacking the finger-loop-region, we show that the two isoforms specifically by proximal and distal C-terminal phosphorylation and in the absence of GPCR kinases (GRKs

type-specific functions Published date November 1, 2022 Abstract G-protein coupled receptor kinases (GRKs However, there is growing evidence that GRKs can also control cellular functions beyond GPCR regulation Immune cells commonly express two to four members of the GRK family (GRK2, GRK3, GRK5, GRK6) simultaneously In particular, we are missing comprehensive studies comparing the role of this GRK interplay for (a) To address this issue, we generated mouse models of single, combinatorial and complete GRK knockouts

initial project to identify and clone taste receptors was unsuccessful, but led to the identification of GRK5 and continued focus on GRKs (particularly GRKs 4,5,6) and arrestins as GPCR regulators and as mediators regulation of G protein-coupled receptor signaling particularly by the G protein-coupled receptor kinase (GRK

initial project to identify and clone taste receptors was unsuccessful, but led to the identification of GRK5 and continued focus on GRKs (particularly GRKs 4,5,6) and arrestins as GPCR regulators and as mediators regulation of G protein-coupled receptor signaling particularly by the G protein-coupled receptor kinase (GRK