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. 2023 Sep 23;14:5938. doi: 10.1038/s41467-023-41646-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — In its constitutively active state (top panel), GPR61 adopts a conformation that allows binding and nucleotide exchange of the G protein complex (bottom left panel) to stimulate cyclic AMP-mediated signaling through activation of adenylate cyclase. Inverse agonist compound 1 (magenta) binds to an intracellular allosteric pocket overlapping that bound by Gαs and acts as a wedge to remodel the flanking helices (yellow arrow), destroying the Gαs-binding pocket and creating direct clashes that prevent potential Gαs binding.