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Concerted action of ENaC, Nedd4-2, and Sgk1 in transepithelial Na(+) transport.
American journal of physiology. Renal physiology
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review - Publication Status: ppublish
The 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.
Aldosterone, Animals, Biological Transport, Calcium-Binding Proteins, Drug Interactions, Epithelial Sodium Channel, Epithelium, Humans, Immediate-Early Proteins, Kidney, Ligases, Nuclear Proteins, Phosphorylation, Protein-Serine-Threonine Kinases, Sodium, Sodium Channels, Ubiquitin-Protein Ligases
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