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

This study revealed that CCR2 scavenging is independent of G proteins, GRKs, arrestins, as well as clathrin from what has been established for other chemokine scavenger receptors that where shown to couple to GRKs

August 2022 GRK2 selectively attenuates the neutrophil NADPH-oxidase response triggered by β-arrestin Among the family of GPCR kinases (GRKs) that regulate receptor phosphorylation and signaling termination , GRK2, which is highly expressed by immune cells, plays an important role. In this study, we investigated the effects of GRK2 inhibitors on neutrophil functions induced by GPR84 GRK2 was shown to be expressed in human neutrophils and analysis of subcellular fractions revealed a

receptors on B cells and intracellular β2-ADR downstream molecules (G protein-coupled receptor kinase 2 (GRK Moreover, we observed a profound downregulation of GRK-2 shortly after induction of arthritis and an

system of the three most important GPCR signaling effectors: heterotrimeric G proteins, GPCR kinases (GRKs

Molecular signature of CCR2 scavenging - no G proteins, no GRKs, no arrestins, and no clathrin Chemokine activation of Gαiβγ, followed by phosphorylation of the receptor C terminus by G protein receptor kinases (GRKs ), specifically GRK2 and GRK3 (A. In this study, the role of these 3 molecular players (G proteins, GRKs, and β-arrestin) is investigated Regarding GRKs role in CCR2 scavenging, BRET, flow cytometry and fluorescence microscopy readouts revealed

A recent focus on GPCR intracellular-regulating proteins such as GPCR kinases (GRKs) has uncovered GRK2 Current literature strongly establishes increased levels and activity of GRK2 in multiple models of CVD Additionally, the GRK2 interactome includes numerous proteins which interact with differential domains of GRK2 to modulate both beneficial and deleterious signaling pathways in the heart, indicating that These data support the premise that GRK2 should be at the forefront of a novel investigative drug search

In this model, GPCR signaling is turned-off by receptor phosphorylation via GPCR kinases (GRKs) and subsequent

Michel Bouvier, J Silvio Gutkind, and team found that Gαs is essential for GRK selectivity and gene regulation cAMP signaling by a polypeptide hormone GPCR Gαs is dispensable for β-arrestin coupling but dictates GRK

., for their work on GRK specificity and Gβγ dependency determines the potential of a GPCR for arrestin-biased protein-coupled receptor kinases in hypertension: physiology, pathogenesis, and therapeutic targets GRK

GPCR kinases (GRKs) and β-arrestins are activated by agonist-bound GPCRs and interact with the receptor Notably, GRKs phosphorylate active GPCRs, enabling high-affinity arrestin binding, which is crucial for Changes in the availability of regulatory proteins like GRKs can impact GPCR phosphorylation and subsequent

Additionally, GLP-1R couple to G protein-coupled receptor kinases (GRKs) and recruit β-arrestins, adding

effector protein recruitment assays (e.g G protein recruitment assay [6], mini-G recruitment assay [7], GRK

GPCR-kinase 3 (GRK3) is critical for GPCR signaling. However, GRK3’s functions and clinical utility in GAC progression and metastases are unknown. Methods We studied GRK3 expression in normal, primary, and metastatic GAC tissues. We identified a novel GRK3 inhibitor, LD2, through a chemical-library screen. Impact of GRK3 on YAP1 and its targets was determined."

we compared the efficacy of seven agonists to induce G protein, G protein-coupled receptor kinase 2 (GRK2 In order to avoid interference between these interactions, we studied GRK2 binding in the presence of We measured substantial differences in the agonist efficacies to induce M3R-arrestin3 versus M3R-GRK2 However, the rank order of the agonists for G protein- and GRK2-M3R interaction was the same, suggesting that G protein and GRK2 binding to M3R requires similar receptor conformations, whereas requirements

receptor functions Signal profiles and spatial regulation of β-arrestin recruitment through Gβ5 and GRK3

of the Receptor-Associated G Proteins in Two Lepidopteran Species GPCRs in Neuroscience Role of the GRK2

Amylin receptor subunit interactions are modulated by agonists and determine signaling Distinct role of GRK3

activated μ-opioid receptor Understanding the impact of nuclear-localized GPCRs on cellular signalling GRK2

., for their research on GRK2 kinases in the primary cilium initiate SMOOTHENED-PKA signaling in the A-Kinase-Anchoring-Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle GRK2

receptor-associated proteins in the caudate and the putamen of cynomolgus macaques following chronic ethanol drinking GRK5

Molecular Insights into GPCR Function Fungal alkaloid malbrancheamide reorients the lipid binding domain of GRK5

protein-coupled receptor GPR52 Endosome positioning coordinates spatially selective GPCR signaling GRK5

Structural studies at high resolution have illuminated the intricate interactions between NTSR1 and GRK2

as a biomarker of oral squamous cell carcinoma (OSCC) by regulating the signaling pathway of miR-19a/GRK6

between GPI-anchored proteins and adhesion GPCRs GPCR Activation and Signaling GPCR activation and GRK2