AKT1 E17K mutant phosphorylates GSK3

Stable Identifier
Reaction [transition]
Homo sapiens
Locations in the PathwayBrowser
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout

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).

Literature References
PubMed ID Title Journal Year
12668767 Stabilization of beta-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth

Haq, S, Walters, B, Kilter, H, Michael, A, Woodgett, J, Force, T, Dotto, P, Bhattacharya, K, Andreucci, M

Proc. Natl. Acad. Sci. U.S.A. 2003
18256540 Activating E17K mutation in the gene encoding the protein kinase AKT1 in a subset of squamous cell carcinoma of the lung

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

Cell Cycle 2008
9478990 Potential role of protein kinase B in insulin-induced glucose transport, glycogen synthesis, and protein synthesis

Yazaki, Y, Kaburagi, Y, Kadowaki, T, Burgering, BM, Yamamoto-Honda, R, Tobe, K, Komuro, I, Ueki, K, Akanuma, Y, Coffer, PJ, Yamauchi, T

J. Biol. Chem. 1998
Catalyst Activity

protein serine/threonine kinase activity of p-T308,S473-AKT1 E17K [cytosol]

Normal reaction
Functional status

Gain of function of p-T308,S473-AKT1 E17K [cytosol]

Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Cite Us!