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- W4387253609 abstract "The vasopressin type 2 receptor (V2R) is an essential GPCR in renal regulation of water homeostasis. Upon stimulation, the V2R activates Gαs and Gαq/11, which is followed by robust recruitment of β-arrestins and receptor internalization into endosomes. Unlike canonical GPCR signaling, the β-arrestin association with the V2R does not terminate Gαs activation, and thus, Gαs-mediated signaling is sustained while the receptor is internalized. Here, we demonstrate that this V2R ability to co-interact with G protein/β-arrestin and promote endosomal G protein signaling is not restricted to Gαs, but also involves Gαq/11. Furthermore, our data implies that β-arrestins potentiate Gαs/Gαq/11 activation at endosomes rather than terminating their signaling. Surprisingly, we found that the V2R internalizes and promote endosomal G protein activation independent of β-arrestins to a minor degree. These new observations challenge the current model of endosomal GPCR signaling and suggest that this event can occur in both β-arrestin-dependent and -independent manners. The vasopressin type 2 receptor promotes dual Gαs and Gαq/11 signaling at early endosomes in β-arrestin-dependent and -independent manners." @default.
- W4387253609 created "2023-10-03" @default.
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- W4387253609 date "2023-10-02" @default.
- W4387253609 modified "2023-10-03" @default.
- W4387253609 title "β-arrestin-dependent and -independent endosomal G protein activation by the vasopressin type 2 receptor" @default.
- W4387253609 doi "https://doi.org/10.7554/elife.87754.2" @default.
- W4387253609 hasPublicationYear "2023" @default.
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