In: Pflügers Archiv - European Journal of Physiology, 2012, vol. 464, no. 4, p. 331-343
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In: Journal of the American Society of Nephrology, 2005, vol. 16, p. 2279
Aldosterone plays a central role in Na⁺ homeostasis by controlling Na⁺ reabsorption in the aldosterone-sensitive distal nephron involving the epithelial Na⁺ channel (ENaC). Part of the effects of aldosterone is mediated by serum and glucocorticoid-induced kinase 1 (Sgk1), a Ser/Thr kinase whose expression is rapidly induced by aldosterone and that increases in heterologous expression...
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In: Histochemistry and Cell Biology, 2005, vol. 123, no. 4-5, p. 335-346
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In: Histochemistry and Cell Biology, 2005, vol. 123(4-5), p. 335
Fibrosis is considered as a central factor in the loss of renal function in chronic kidney diseases. The origin of fibroblasts and myofibroblasts that accumulate in the interstitium of the diseased kidney is still a matter of debate. It has been shown that accumulation of myofibroblasts in inflamed and fibrotic kidneys is associated with upregulation of fibroblast-specific protein 1 (FSP1,...
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In: Pflügers Archiv : European Journal of Physiology, ///-
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In: Journal of the American Society of Nephrology, 2006, vol. 17, p. 1264-1274
The activity of the epithelial sodium (Na⁺) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) needs to be tightly regulated to match urinary Na⁺ excretion with dietary Na⁺ intake. The ubiquitin-protein ligase Nedd4-2, which in vitro interacts with ENaC subunits and reduces ENaC cell surface abundance and activity by ubiquitylation of the channel, may participate in...
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In: Pflügers Archiv - European Journal of Physiology, 2015, vol. 467, no. 12, p. 2529-2539
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In: Journal of the American Society of Nephrology, 2010, vol. 21, p. -
Lithium-induced nephrogenic diabetes insipidus (NDI) is accompanied by polyuria, downregulation of aquaporin 2 (AQP2), and cellular remodeling of the collecting duct (CD). The amiloride-sensitive epithelial sodium channel (ENaC) is a likely candidate for lithium entry. Here, we subjected transgenic mice lacking αENaC specifically in the CD (knockout [KO] mice) and littermate controls to chronic...
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In: The Journal of Clinical Investigation, 2005, vol. 115(6), p. 1651
Thiazide diuretics enhance renal Na⁺ excretion by blocking the Na⁺-Cl⁻ cotransporter (NCC), and mutations in NCC result in Gitelman syndrome. The mechanisms underlying the accompanying hypocalciuria and hypomagnesemia remain debated. Here, we show that enhanced passive Ca²⁺ transport in the proximal tubule rather than active Ca²⁺ transport in distal convolution explains...
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In: Journal of the American Society of Nephrology, 2005, vol. 16, p. 3175
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