Salt, sodium channels, and SGK1
Copyright policy )Salt, sodium channels, and SGK1
The hormone aldosterone increases extracellular fluid volume and blood pressure by activating epithelial Na+ channels (ENaCs). Serum- and glucocorticoid-induced kinase 1 (SGK1) is an aldosterone-stimulated signaling molecule that enhances distal nephron Na+ transport, in part by preventing the internalization of ENaCs from the plasma membrane. In this issue of the JCI, Zhang et al. demonstrate that SGK1 enhances transcription of the alpha subunit of ENaC by preventing histone methylation, providing an additional mechanism by which SGK1 increases ENaC-mediated Na+ transport in the distal nephron (see the related article beginning on page 773).
- University of California, San Francisco United States
- Columbia University United States
Transcription, Genetic, Nephrons, Protein Serine-Threonine Kinases, Sodium Chloride, Methylation, Immediate-Early Proteins, Histones, Mice, Protein Transport, Receptors, Mineralocorticoid, Gene Expression Regulation, Animals, Humans, Epithelial Sodium Channels, Aldosterone
Transcription, Genetic, Nephrons, Protein Serine-Threonine Kinases, Sodium Chloride, Methylation, Immediate-Early Proteins, Histones, Mice, Protein Transport, Receptors, Mineralocorticoid, Gene Expression Regulation, Animals, Humans, Epithelial Sodium Channels, Aldosterone
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