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 α 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).
David Pearce, Thomas R. Kleyman
Title and authors | Publication | Year |
---|---|---|
Role of Epithelial Sodium Channels and Their Regulators in Hypertension*
R Soundararajan, D Pearce, RP Hughey, TR Kleyman |
The Journal of biological chemistry | 2010 |
Regulation of the epithelial sodium channel (ENaC) by membrane trafficking
MB Butterworth |
Biochimica et Biophysica Acta | 2010 |
Insulin activates epithelial sodium channel (ENaC) via phosphoinositide 3-kinase in mammalian taste receptor cells
AF Baquero, TA Gilbertson |
AJP Cell Physiology | 2010 |