A5012205368- Electrolyte and hormonal disorders
- Ion Transport and Channel Regulation
- Genetic and Kidney Cyst Diseases
- Hydrogen Storage and Materials
- Microtubule and mitosis dynamics
- Pancreatic function and diabetes
- Erythrocyte Function and Pathophysiology
- Birth, Development, and Health
- Potassium and Related Disorders
Max Delbrück Center
2019-2022
Technische Universität Berlin
2022
Significance Statement Dysregulation of vasopressin-induced water reabsorption in the renal collecting duct leads to diabetes insipidus, a congenital or acquired syndrome. Some forms insipidus lack effective treatments prevent excessive loss hypotonic urine that characterizes condition. The authors previously identified antimycotic drug fluconazole as potential therapy, acting modulate effects channel protein aquaportin-2 (AQP2). In this study, they show vitro and vivo induces...
The cAMP-dependent aquaporin-2 (AQP2) redistribution from intracellular vesicles into the plasma membrane of renal collecting duct principal cells induces water reabsorption and fine-tunes body homeostasis. However, mechanisms controlling localization AQP2 are not understood in detail. Using immortalized mouse medullary (MCD4) primary rat inner (IMCD) as model systems, we here discovered a key regulatory role Aurora kinase A (AURKA) control AQP2. AURKA-selective inhibitor Aurora-A I novel...
Congenital nephrogenic diabetes insipidus (NDI) is a rare hereditary disease characterized by excessive diuresis and compensatory polydipsia. No causal treatment of NDI exists, leaving the patient with severe symptoms, impaired quality life, at risk mental impairment due to recurrent dehydration episodes in childhood. In ~90% cases, caused sequence variants AVPR2 gene. This gene located on X-chromosome encodes vasopressin V2 receptor1,2 (V2R).
Abstract Vasopressin-mediated water reabsorption from primary urine in the renal collecting duct is essential for regulating body homeostasis and depends on channel aquaporin-2 (AQP2). Dysregulation of process can cause balance disorders. Here, we present cell-based high-throughput screenings to identify proteins small molecules as tools elucidate molecular mechanisms underlying AQP2 control potential starting points development disorder drugs.