Aldosterone-induced Sgk1 relieves Dot1a-Af9–mediated transcriptional repression of epithelial Na+ channel α-Reference-Cited by-同舟云学术

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Aldosterone-induced Sgk1 relieves Dot1a-Af9–mediated transcriptional repression of epithelial Na+ channel α

Published:2007-03-01 Issue:3 Volume:117 Page:773-783
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:J. Clin. Invest.

Author:

Zhang Wenzheng,Xia Xuefeng,Reisenauer Mary Rose,Rieg Timo,Lang Florian,Kuhl Dietmar,Vallon Volker,Kone Bruce C.

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Reference38 articles.

1. New insights into epithelial sodium channel function in the kidney: site of action, regulation by ubiquitin ligases, serum- and glucocorticoid-inducible kinase and proteolysis

2. Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na+ channel cell surface expression

3. Aldosterone-induced increase in the abundance of Na+ channel subunits

4. Glucocorticoid Induction of Epithelial Sodium Channel Expression in Lung and Renal Epithelia Occurs via trans-Activation of a Hormone Response Element in the 5′-Flanking Region of the Human Epithelial Sodium Channel α Subunit Gene

5. Gene regulation of ENaC subunits by serum- and glucocorticoid-inducible kinase-1

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