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This Article Full Text Full Text (PDF) All Versions of this Article: 292/4/F1219    most recent 00214.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Holzman, J. L. Articles by Eaton, D. C. Search for Related Content PubMed PubMed Citation Articles by Holzman, J. L. Articles by Eaton, D. C.

Transactivation of the IGF-1R by aldosterone

¹Center for Cell and Molecular Signaling, Department of Physiology, Emory University School of Medicine, and ²Graduate Program in Biochemistry, Cell, and Developmental Biology, Emory University Graduate School of Arts and Sciences, Atlanta, Georgia

Submitted 13 June 2006 ; accepted in final form 20 December 2006

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.

PI3-kinase; insulin-like growth factor-1; Akt; A6 cells

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