Go to
JCI Insight
Citations to this article
David Pearce, Thomas R. Kleyman
Published March 1, 2007
Citation Information: J Clin Invest. 2007;117(3):592-595. https://doi.org/10.1172/JCI31538.
Citation Information: J Clin Invest. 2007;117(3):592-595. https://doi.org/10.1172/JCI31538.
Abstract
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).
Authors
David Pearce, Thomas R. Kleyman
Total citations by year
Citation information
Citations to this article in year 2019 (1)
| Title and authors | Publication | Year |
|---|---|---|
|
Trichostatin A blocks aldosterone‐induced Na + transport and control of serum‐ and glucocorticoid‐inducible kinase 1 in cortical collecting duct cells
MK Mansley, AJ Roe, SL Francis, JH Gill, MA Bailey, SM Wilson |
British Journal of Pharmacology | 2019 |
Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)