Introduction of AQP2
AQP2 (aquaporin-2), encoded by AQP2 gene, is a member of the aquaporin family. Along with several other members, AQP2 gene is clustered together on chromosome 12q13. AQP2 is mainly expressed in the renal collecting duct epithelial cells and in intracellular vesicles located throughout the cell, where AQP2 participates in the reabsorption of water molecules from the urine by the renal collecting duct. Abnormal function or mutations of AQP2 have been linked to autosomal dominant and recessive forms of nephrogenic diabetes insipidus or kidney cyst.
|Basic Information of AQP2|
ADH water channel, Aquaporin-CD, AQP-CD, Collecting duct water channel protein
WCH-CD, Water channel protein for renal collecting duct
|Organism||Homo sapiens (Human)|
Function of AQP2 Membrane Protein
V2R and AQP2 are the major regulators of urine concentration. Phosphorylated by cAMP-dependent protein kinase PKA, AQP2 can move to the apical membrane, which causes water to be reabsorbed from the urine through the AQP2 water channel, thereby improving the body's dehydration state. It has shown that several serine, mainly include 256 (S256), 261 (S261) and 269 (S269) residing in the C-terminal of AQP2, have been identified as major phosphorylation sites associated with AQP2 trafficking. Mutations in AQP2 are associated with multiple diseases, such as Diabetes Insipidus, Nephrogenic, Autosomal and Diabetes Insipidus, Nephrogenic, X-Linked phenotype. Measuring urinary excretion of AQP2 is of value in diagnosing central diabetes insipidus. Innocuous nephrogenic diabetes insipidus (NDI) patients do not respond to vasopressin kidneys or AQP2 dysfunction can impair AQP2 activity and water reabsorption, leading to polyuria.
Fig.1 The mechanisms of urine concentration by vasopressin.
Fig.2 The mechanisms of urine concentration by Wnt5a.
Application of AQP2 Membrane Protein in Literature
In this article, the authors conduct an overview of novel therapeutic molecules of congenital nephrogenic diabetes insipidus (NDI). These molecules can activate AQP2 by bypassing defective V2R signaling with a particular focus on the activators of the calcium and cAMP signaling pathways.
This article indicates that the low molecular weight compound 3,3'-diamino-4,4'-dihydroxydiphenylmethane (FMP-API-1) and its derivatives can increase AQP2 activity to the same extent as vasopressin, and increase urine osmolality in the context of V2R inhibition, suggesting that FMP-API-1 may be a promising therapy for the treatment of congenital NDI caused by V2R mutations.
This article firstly shows that steviol can slow cyst growth by reducing AQP2 transcription, and promote proteasome, as well as lysosome-mediated AQP2 degradation.
This article reveals that AQP2 is a key molecule that determines the urine concentrating ability of the kidney. AQP2 is deeply involved in water-balance disorders such as water retention in heart failure and liver cirrhosis, indicating that it could be a useful biomarker for diagnosis and prognosis of such diseases.
This report shows that CaSR signaling can reduce AQP2 abundance both via AQP2-targeting miRNA-137 and the p38-MAPK/AQP2-pS261/ubiquitination/proteasomal axis.
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