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. 2020 Oct 2;10:16383. doi: 10.1038/s41598-020-73089-x

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Rescue of ER-retained V2R mutants by tolvaptan. (A) Maturation of WT, L86P, M272R and W323_I324insR-V2R after treatment with 1 μM tolvaptan for 16 h. Cells were lysed and analysed by immunoblotting using anti-GFP antibody. Tolvaptan was effective in ameliorating the glycosylation maturation of M272R mutants. (B) Representative pictures of M272R-V2R-GFP in polarized MDCK cells showed restoration of basolateral membrane expression of M272R after treatment with tolvaptan. (C) Generation of cAMP in MDCK cells stably expressing M272R variant treated with or without tolvaptan and following dDAVP stimulation. M272-expressing MDCK cells treated with tolvaptan showed significantly increased level of cAMP after stimulation with dDAVP. Values are means ± SEM (n = 4, *P < 0.05; one-way ANOVA).