GRK5 regulates endocytosis of FPR2 independent of β-arrestins.

ABSTRACT: The formyl-peptide receptor 2 (FPR2) is a G-protein-coupled receptor that responds to pathogen-derived peptides and regulates both proinflammatory and proresolution cellular processes. While ligand selectivity and G-protein signaling of FPR2 have been well characterized, molecular mechanisms controlling subsequent events such as endocytosis and recycling to the plasma membrane are less understood. Here, we show the key role of the G-protein-coupled receptor kinase 5 (GRK5) in facilitating FPR2 endocytosis and postendocytic trafficking. We found, in response to activation by a synthetic peptide WKYMVm, the recruitment of β-arrestins to the receptor requires both putative phosphorylation sites in the C-terminal region of FPR2 and the presence of GRKs, predominantly GRK5. Furthermore, althoug

SUBMITTER: Jack CE 

PROVIDER: S-EPMC11773488 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature