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 |
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Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptor-dependent pathway
Shigeru Shibata, Shengyu Mu, Hiroo Kawarazaki, Kazuhiko Muraoka, Ken-ichi Ishizawa, Shigetaka Yoshida, Wakako Kawarazaki, Maki Takeuchi, Nobuhiro Ayusawa, Jun Miyoshi, Yoshimi Takai, Akira Ishikawa, Tatsuo Shimosawa, Katsuyuki Ando, Miki Nagase, Toshiro Fujita |
Journal of Clinical Investigation | 2011 |
The role of the ENaC-regulatory complex in aldosterone-mediated sodium transport
R Soundararajan, D Pearce, T Ziera |
Molecular and Cellular Endocrinology | 2011 |