Akt participation in the Wnt signaling pathway through Dishevelled |
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Authors: | Fukumoto S Hsieh C M Maemura K Layne M D Yet S F Lee K H Matsui T Rosenzweig A Taylor W G Rubin J S Perrella M A Lee M E |
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Affiliation: | Cardiovascular and Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital and the Cardiovascular Research Center Harvard Medical School, Boston, Massachusetts 02115, USA. |
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Abstract: | Inactivation of glycogen synthase kinase 3beta (GSK3beta) and the resulting stabilization of free beta-catenin are critical steps in the activation of Wnt target genes. While Akt regulates GSK3alpha/beta in the phosphatidylinositide 3-OH kinase signaling pathway, its role in Wnt signaling is unknown. Here we report that expression of Wnt or Dishevelled (Dvl) increased Akt activity. Activated Akt bound to the Axin-GSK3beta complex in the presence of Dvl, phosphorylated GSK3beta and increased free beta-catenin levels. Furthermore, in Wnt-overexpressing PC12 cells, dominant-negative Akt decreased free beta-catenin and derepressed nerve growth factor-induced differentiation. Therefore, Akt acts in association with Dvl as an important regulator of the Wnt signaling pathway. |
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