Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells |
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Authors: | Kim Sung-Eun Cho Jae-Young Kim Kyung-Sup Lee Su-Jae Lee Ki-Hoo Choi Kang-Yell |
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Institution: | Department of Biotechnology, Division of Cellular and Molecular Biology, Yonsei University, 132 Shinchon-Dong, Seodemun-Gu, Seoul 120-752, South Korea. |
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Abstract: | 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. |
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