AKT1 E17K gain-of-function mutant preserves the ability to phosphorylate GSK3 (Malanga et al. 2008). AKT-mediated phosphorylation inactivates GSK3 and enables WNT-independent stabilization of beta-catenin (CTNNB1) (Haq et al. 2003). AKT-mediated inactivation of GSK3 also triggers changes in glucose metabolism (Ueki et al. 1997).
Haq, S, Walters, B, Kilter, H, Michael, A, Woodgett, J, Force, T, Dotto, P, Bhattacharya, K, Andreucci, M
Franco, R, De Rosa, N, Rocco, G, Savino, R, Malara, N, Malanga, D, Fabiani, F, Pirozzi, G, Scrima, M, De Marco, C, Tirino, V, De Gisi, S, Chiappetta, G, Viglietto, G
Yazaki, Y, Kaburagi, Y, Kadowaki, T, Burgering, BM, Yamamoto-Honda, R, Tobe, K, Komuro, I, Ueki, K, Akanuma, Y, Coffer, PJ, Yamauchi, T
protein serine/threonine kinase activity of p-T308,S473-AKT1 E17K [cytosol]
Gain of function of p-T308,S473-AKT1 E17K [cytosol]
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