Am J Physiol Renal Physiol 2007 Apr 01;2924:F1219-28. doi: 10.1152/ajprenal.00214.2006.

Transactivation of the IGF-1R by aldosterone.

???displayArticle.abstract???
Activation of epithelial sodium channels (ENaC) by aldosterone, insulin, or insulin-like growth factor-1 (IGF-1) in renal epithelial cells (including the Xenopus laevis renal cell line A6) appears to share some common signaling elements subsequent to the initial insulin or IGF-1 receptor activation. Previously, the convergence point for insulin or IGF-1 and aldosterone signaling was assumed to be downstream of the receptor at the level of phosphatidylinositol 3-kinase (PI3-K); however, this study shows aldosterone directly transactivates the IGF-1 receptor (IGF-1R). In A6 cells, 10-min exposure to aldosterone increased the phosphorylation of the IGF-1 receptor, insulin receptor substrate-1 (IRS-1), and Akt (PKB). Furthermore, aldosterone activated PI3-K and phosphorylation of the most downstream element, Akt, was blocked by the specific PI3-K inhibitor LY-294002. Transactivation requires aldosterone binding to the mineralocorticoid/glucocorticoid receptor and does not require transcription.

???displayArticle.pubmedLink??? 17190911
???displayArticle.link??? Am J Physiol Renal Physiol
???displayArticle.grants??? [+]

Species referenced: Xenopus laevis
Genes referenced: akt1 igf1r ins