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lüll Concerted action of ENaC, Nedd4-2, and Sgk1 in transepithelial Na(+) transport Kamynina E; Staub OAm J Physiol Renal Physiol 2002[Sep]; 283 (3): F377-87The epithelial Na(+) channel (ENaC), located in the apical membrane of renal aldosterone-responsive epithelia, plays an essential role in controlling the Na(+) balance of extracellular fluids and hence blood pressure. As of now, ENaC is the only Na(+) transport protein for which genetic evidence exists for its involvement in the genesis of both hypertension (Liddle's syndrome) and hypotension (pseudohypoaldosteronism type 1). The regulation of ENaC involves a variety of hormonal signals (aldosterone, vasopressin, insulin), but the molecular mechanisms behind this regulation are mostly unknown. Two regulatory proteins have gained interest in recent years: the ubiquitin-protein ligase neural precursor cell-expressed, developmentally downregulated gene 4 isoform Nedd4-2, which negatively controls ENaC cell surface expression, and serum glucocorticoid-inducible kinase 1 (Sgk1), which is an aldosterone- and insulin-dependent, positive regulator of ENaC density at the plasma membrane. Here, we summarize present ideas about Sgk1 and Nedd4-2 and the lines of experimental evidence, suggesting that they act sequentially in the regulatory pathways governed by aldosterone and insulin and regulate ENaC number at the plasma membrane.|*Nuclear Proteins[MESH]|*Ubiquitin-Protein Ligases[MESH]|Aldosterone/pharmacology[MESH]|Animals[MESH]|Biological Transport[MESH]|Calcium-Binding Proteins/*physiology[MESH]|Drug Interactions[MESH]|Endosomal Sorting Complexes Required for Transport[MESH]|Epithelial Sodium Channels[MESH]|Epithelium/metabolism[MESH]|Humans[MESH]|Immediate-Early Proteins[MESH]|Kidney/metabolism[MESH]|Ligases/*physiology[MESH]|Nedd4 Ubiquitin Protein Ligases[MESH]|Phosphorylation[MESH]|Protein Serine-Threonine Kinases/*physiology[MESH]|Sodium Channels/*physiology[MESH]|Sodium/*metabolism[MESH] |