Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells

Sung Eun Kim; Jae Young Cho; Kyung Sup Kim; Su Jae Lee; Ki Hoo Lee; Kang Yell Choi

doi:10.1016/j.cellsig.2004.04.004

Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells

Sung Eun Kim, Jae Young Cho, Kyung Sup Kim, Su Jae Lee, Ki Hoo Lee, Kang Yell Choi

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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.

Original language	English
Pages (from-to)	1309-1317
Number of pages	9
Journal	Cellular Signalling
Volume	16
Issue number	11
DOIs	https://doi.org/10.1016/j.cellsig.2004.04.004
Publication status	Published - 2004 Nov

Bibliographical note

Funding Information:
This work was supported by grants from The Molecular and Cellular BioDiscovery Research Program (M1-0311-00-0111), the Korea Research Foundation Grant (KRF-2003-2003-015-C00400), and the Korea Science and Engineering Foundation through the Protein Network Research Center at Yonsei University to K.Y. Choi.

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Cell Biology

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10.1016/j.cellsig.2004.04.004

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title = "Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells",

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.",

author = "Kim, {Sung Eun} and Cho, {Jae Young} and Kim, {Kyung Sup} and Lee, {Su Jae} and Lee, {Ki Hoo} and Choi, {Kang Yell}",

note = "Funding Information: This work was supported by grants from The Molecular and Cellular BioDiscovery Research Program (M1-0311-00-0111), the Korea Research Foundation Grant (KRF-2003-2003-015-C00400), and the Korea Science and Engineering Foundation through the Protein Network Research Center at Yonsei University to K.Y. Choi.",

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AU - Lee, Su Jae

AU - Lee, Ki Hoo

AU - Choi, Kang Yell

N1 - Funding Information: This work was supported by grants from The Molecular and Cellular BioDiscovery Research Program (M1-0311-00-0111), the Korea Research Foundation Grant (KRF-2003-2003-015-C00400), and the Korea Science and Engineering Foundation through the Protein Network Research Center at Yonsei University to K.Y. Choi.

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N2 - 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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Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells

Abstract

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