Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells.
We have characterized the role of Drosophila PI3K and AKT in ERK pathway activation involving insulin-induced proliferation using Drosophila Schneider cells. After insulin treatment, dPI3K and dAKT activities were both increased along with activation of the dERK pathway components dMEK and dERK. The insulin-induced activations of dERK and dAKT were blocked by LY294002, dPTEN, and by an AKT inhibitor, indicating involvement of dPI3K and dAKT in the insulin-induced dERK and dAKT activations. Proliferation and the G1 to S phase cell cycle progression due to insulin were also blocked by PI3K and AKT inhibitors, indicating that the Drosophila PI3K-AKT pathway involves insulin-mediated cell proliferation. The insulin-stimulated size increase was blocked by both LY294002 and AKT inhibitor, not by U0126, indicating that insulin-mediated size control by dPI3K and dAKT occurs independently of the ERK pathway. This study indicates that dPI3K and dAKT are involved in insulin-induced ERK pathway activation leading to proliferation in Drosophila Schneider cells.[1]References
- Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells. Kim, S.E., Cho, J.Y., Kim, K.S., Lee, S.J., Lee, K.H., Choi, K.Y. Cell. Signal. (2004) [Pubmed]
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