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• W4281293885 abstract "PEN is an abundant neuropeptide that activates G protein-coupled receptor 83 (GPR83), which is considered a novel therapeutic target due to its roles in regulation of feeding-, reward-, and anxiety-related behaviors. The major form of PEN in the brain is 22 residues in length. Previous studies have identified shorter forms of PEN in mouse brain and neuroendocrine cells; these shorter forms were named PEN18, PEN19, and PEN20, with the number reflecting the length of the peptide. The C-terminal five residues of PEN20 are identical to the C-terminus of a procholecystokinin (proCCK)-derived peptide, named proCCK56-62, that is present in mouse brain. ProCCK56-62 is highly conserved across species, although it has no homology to the bioactive cholecystokinin domain. ProCCK56-62 and a longer form, proCCK56-63, were tested for their ability to engage GPR83. Both peptides bind GPR83 with high affinity, activate second messenger pathways, and induce ligand-mediated receptor endocytosis. Interestingly, the shorter PEN peptides, ProCC56-62 and ProCCK56-63, differentially activate signal transduction pathways. Whereas PEN22 and PEN20 facilitate receptor coupling to G<i>α</i>i, PEN18, PEN19, and ProCCK peptides facilitate coupling to G<i>α</i>s. Furthermore, the ProCCK peptides exhibit dose-dependent G<i>α</i> subtype selectivity in that they facilitate coupling to G<i>α</i>s at low concentrations and G<i>α</i>i at high concentrations. These data demonstrate that peptides derived from two distinct peptide precursors can differentially activate GPR83 and that GPR83 exhibits G<i>α</i> subtype preference depending on the nature and concentration of the peptide. These results are consistent with the emerging idea that endogenous neuropeptides function as biased ligands. <h3>SIGNIFICANCE STATEMENT</h3> We found that peptides derived from procholecystokinin (proCCK) bind and activate G protein-coupled receptor 83, which is known to bind peptides derived from proSAAS. Different forms of the proCCK- and proSAAS-derived peptides show biased agonism, activating Gαs or Gαi depending on the length of the peptide and/or its concentration." @default.
• W4281293885 created "2022-05-24" @default.
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• W4281293885 date "2022-05-23" @default.
• W4281293885 modified "2023-10-17" @default.
• W4281293885 title "GPR83 Engages Endogenous Peptides from Two Distinct Precursors to Elicit Differential Signaling" @default.
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• W4281293885 doi "https://doi.org/10.1124/molpharm.122.000487" @default.
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