ArticleFrontiers in pharmacology2022
Functional Rescue of a Nephrogenic Diabetes Insipidus Causing Mutation in the V2 Vasopressin Receptor by Specific Antagonist and Agonist Pharmacochaperones.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- A small molecule stabilizer rescues the surface expression of nearly all missense variants in a GPCR.Nature structural & molecular biology · 2025Article
- The natural history of untreated X-linked nephrogenic diabetes insipidus with mutation in the vasopressin V2 receptor gene.CEN case reports · 2025Article
- Nephrogenic Diabetes Insipidus Affecting Three Males in Two Generations-Case Report and Review of the Literature.Children (Basel, Switzerland) · 2025Article
- Non-canonical Golgi-compartmentalized Gβγ signaling: mechanisms, functions, and therapeutic targets.Trends in pharmacological sciences · 2023Review
- V2 vasopressin receptor mutations: future personalized therapy based on individual molecular biology.Frontiers in endocrinology · 2023Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
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Abstract
The urine concentrating function of the kidney is essential to maintain the water homeostasis of the human body. It is mainly regulated by the arginine-vasopressin (AVP), which targets the type 2 vasopressin receptor (V2R) in the kidney. The inability of V2R to respond to AVP stimulation leads to decreased urine concentration and congenital nephrogenic diabetes insipidus (NDI). NDI is characterized by polyuria, polydipsia, and hyposthenuria. In this study, we identified a point mutation (S127F) in the
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