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V2 vasopressin receptor mutations. | LitMetric

V2 vasopressin receptor mutations.

Vitam Horm

Department of Endocrinology and Nephrology, The University of Tokyo, Tokyo, Japan; Department of Pharmacology, St. Marianna University School of Medicine, Kawasaki, Japan. Electronic address:

Published: June 2021

AI Article Synopsis

  • V2 vasopressin receptor (V2R) is linked to diseases through mutations that can either hinder or enhance its function, specifically affecting water balance in the body.
  • Loss-of-function mutations lead to nephrogenic diabetes insipidus (NDI), while gain-of-function mutations result in nephrogenic syndrome of inappropriate antidiuresis (NSIAD).
  • The study of V2R mutations indicates complex functional mechanisms and suggests new treatment possibilities, including pharmacochaperones for NDI and inverse agonists for NSIAD, while also enhancing our understanding of GPCR roles and mechanisms.

Article Abstract

V2 vasopressin receptor (V2R) is a member of the G protein-coupled receptor (GPCR) family in which many disease-causing mutations have been identified and thus generated much interest. Loss-of-function V2R mutations cause nephrogenic diabetes insipidus (NDI) whereas gain-of-function mutations cause nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The mechanisms underlying a V2R loss-of-function can be theoretically classified as either protein expression, localization (ER retention) or functional disorders. Functional analyses have revealed however that these mechanisms are likely to be complex. Strikingly, V2R mutations at the same site can result in opposite phenotypes, e.g., R137H and R137L/C cause NDI and NSIAD, respectively. These findings support the notion that the constitutive activation of GPCRs might be often associated with their instability and denaturation. Thus, functional analysis of disease-causing V2R mutations may not only reveal potential new treatment strategies using pharmacochaperones for NDI and inverse agonists for NSIAD, but also provide a greater understanding of the physiological functions of GPCRs and highlight the new paradigms, i.e., biased agonism and protean agonism.

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Source
http://dx.doi.org/10.1016/bs.vh.2019.08.012DOI Listing

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