ArticleMolecular biology of the cell2017
Differential phosphorylation signals control endocytosis of GPR15.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- The Biological and Clinical Relevance of G Protein-Coupled Receptors to the Outcomes of Hematopoietic Stem Cell Transplantation: A Systematized Review.International journal of molecular sciences · 2019Pooled it
- GPR15-guided CD8Nature · 2026Article
- Subcellular Redistribution of Endomembrane GPR15 Promotes NAD+-Mediated Metabolic Reprogramming and Boosts 5-FU Chemosensitivity in Colorectal Cancer.Cancer research · 2026Article
- Prognostic value assessment and in vitro validation of mitochondria-ferroptosis-related genes in multiple myeloma.Scientific reports · 2025Article
- Emerging roles of a chemoattractant receptor GPR15 and ligands in pathophysiology.Frontiers in immunology · 2023Review
- Delineation of the GPR15 receptor-mediated Gα protein signalling profile in recombinant mammalian cells.Basic & clinical pharmacology & toxicology · 2022Article
- QR code model: a new possibility for GPCR phosphorylation recognition.Cell communication and signaling : CCS · 2022Review
- Amino acid starvation-induced LDLR trafficking accelerates lipoprotein endocytosis and LDL clearance.EMBO reports · 2022Article
- The Role of GPR15 Function in Blood and Vasculature.International journal of molecular sciences · 2021Review
- Tyrosine sulfation and O-glycosylation of chemoattractant receptor GPR15 differentially regulate interaction with GPR15L.Journal of cell science · 2021Article
- CX-4945 Induces Methuosis in Cholangiocarcinoma Cell Lines by a CK2-Independent Mechanism.Cancers · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
GPR15 is an orphan G protein-coupled receptor (GPCR) that serves for an HIV coreceptor and was also recently found as a novel homing receptor for T-cells implicated in colitis. We show that GPR15 undergoes a constitutive endocytosis in the absence of ligand. The endocytosis was clathrin dependent and partially dependent on β-arrestin in HEK293 cells, and nearly half of the internalized GPR15 receptors were recycled to the plasma membrane. An Ala mutation of the distal C-terminal Arg-354 or Ser-357, which forms a consensus phosphorylation site for basophilic kinases, markedly reduced the endocytosis, whereas phosphomimetic mutation of Ser-357 to Asp did not. Ser-357 was phosphorylated in vitro by multiple kinases, including PKA and PKC, and pharmacological activation of these kinases enhanced both phosphorylation of Ser-357 and endocytosis of GPR15. These results suggested that Ser-357 phosphorylation critically controls the ligand-independent endocytosis of GPR15. The functional role of Ser-357 in endocytosis was distinct from that of a conserved Ser/Thr cluster in the more proximal C-terminus, which was responsible for the β-arrestin- and GPCR kinase-dependent endocytosis of GPR15. Thus phosphorylation signals may differentially control cell surface density of GPR15 through endocytosis.
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Registered trials
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