Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus | Zendy

Christiane Trimpert | Zendy; Dennis T. M. van den Berg | Zendy; Robert A. Fenton | Zendy; Enno Klußmann | Zendy; Peter M.T. Deen | Zendy

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Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus

Author(s) -

Christiane Trimpert,

Dennis T. M. van den Berg,

Robert A. Fenton,

Enno Klußmann,

Peter M.T. Deen

Publication year - 2012

Publication title -

nephrology dialysis transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.654

H-Index - 168

eISSN - 1460-2385

pISSN - 0931-0509

DOI - 10.1093/ndt/gfs292

Subject(s) - aquaporin 2 , nephrogenic diabetes insipidus , vasopressin , phosphorylation , endocrinology , arginine vasopressin receptor 2 , medicine , polyuria , diabetes insipidus , microbiology and biotechnology , apical membrane , biology , biochemistry , water channel , diabetes mellitus , membrane , mechanical engineering , receptor , antagonist , engineering , inlet

Mutations in the aquaporin-2 (AQP2) gene cause nephrogenic diabetes insipidus (NDI), a renal disorder characterized by polyuria due to a lacking antidiuretic response to vasopressin. While most AQP2 mutants in recessive NDI are misfolded and retained in the endoplasmic reticulum, AQP2-P262L in NDI was impaired in its vasopressin-dependent translocation from vesicles to the plasma membrane.

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