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Article

Functional rescue of vasopressin V2 receptor mutants in MDCK cells by pharmacochaperones: relevance to therapy of nephrogenic diabetes insipidus.

American journal of physiology. Renal physiology - 1 Jan 2007

Robben J H, Sze M, Knoers N V A M, Deen P M T

Abstract excerpt

Intracellular retention of a functional vasopressin V2 receptor (V2R) is a major cause of congenital nephrogenic diabetes insipidus (NDI) and rescue of V2R mutants by nonpeptide antagonists may restore their basolateral membrane (BM) localization and function. However, the criteria for efficient functional rescue of G protein-coupled receptor (GPCR) mutants at clinically feasible antagonist concentrations are...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 16926443
DOI: 10.1152/ajprenal.00247.2006

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AVP

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Functional rescue of vasopressin V2 receptor mutants in MDCK cells by pharmacochaperones: relevance to therapy of nephrogenic diabetes insipidus.PMID 16926443Read ↗

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