ArticleNature communications2018
AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- LRBA organizes distinct vesicular trafficking systems in distal nephron segments for water and sodium conservation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A-Kinase-Anchoring Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle.American journal of respiratory cell and molecular biology · 2025Article
- ZNF185 prevents stress fiber formation through the inhibition of RhoA in endothelial cells.Communications biology · 2023Article
- Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023Article
- Bioinformatics analysis and identification of genes and pathways involved in patients with Wilms tumor.Translational cancer research · 2022Article
- LRBA is essential for urinary concentration and body water homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Molecular mechanisms governing aquaporin relocalisation.Biochimica et biophysica acta. Biomembranes · 2022Review
- Updates and Perspectives on Aquaporin-2 and Water Balance Disorders.International journal of molecular sciences · 2021Review
- Aquaporin 2 regulation: implications for water balance and polycystic kidney diseases.Nature reviews. Nephrology · 2021Review
- Activation of AQP2 water channels by protein kinase A: therapeutic strategies for congenital nephrogenic diabetes insipidus.Clinical and experimental nephrology · 2021Review
- Review
- Nephrogenic diabetes insipidus induced by ureter obstruction due to benign prostatic hyperplasia: A case report.Medicine · 2020Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- Decreased Excretion of Urinary Exosomal Aquaporin-2 in a Puromycin Aminonucleoside-Induced Nephrotic Syndrome Model.International journal of molecular sciences · 2020Article
- Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020Review
- Osmotic diuresis by SGLT2 inhibition stimulates vasopressin-induced water reabsorption to maintain body fluid volume.Physiological reports · 2020Article
- Small molecules for modulating the localisation of the water channel aquaporin-2-disease relevance and perspectives for targeting local cAMP signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2019Review
- Tolvaptan activates the Nrf2/HO-1 antioxidant pathway through PERK phosphorylation.Scientific reports · 2019Article
- Fluconazole Increases Osmotic Water Transport in Renal Collecting Duct through Effects on Aquaporin-2 Trafficking.Journal of the American Society of Nephrology : JASN · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital nephrogenic diabetes insipidus (NDI) is characterized by the inability of the kidney to concentrate urine. Congenital NDI is mainly caused by loss-of-function mutations in the vasopressin type 2 receptor (V2R), leading to impaired aquaporin-2 (AQP2) water channel activity. So far, treatment options of congenital NDI either by rescuing mutant V2R with chemical chaperones or by elevating cyclic adenosine monophosphate (cAMP) levels have failed to yield effective therapies. Here we show that inhibition of A-kinase anchoring proteins (AKAPs) binding to PKA increases PKA activity and activates AQP2 channels in cortical collecting duct cells. In vivo, the low molecular weight compound 3,3'-diamino-4,4'-dihydroxydiphenylmethane (FMP-API-1) and its derivatives increase AQP2 activity to the same extent as vasopressin, and increase urine osmolality in the context of V2R inhibition. We therefore suggest that FMP-API-1 may constitute a promising lead compound for the treatment of congenital NDI caused by V2R mutations.
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