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

Research output: Contribution to journalArticle

21 Citations (Scopus)

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 languageEnglish
Pages (from-to)1309-1317
Number of pages9
JournalCellular Signalling
Volume16
Issue number11
DOIs
Publication statusPublished - 2004 Nov 1

Fingerprint

MAP Kinase Signaling System
Phosphatidylinositol 3-Kinases
Drosophila
Insulin
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
S Phase
Cell Cycle
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Cell Biology

Cite this

Kim, Sung Eun ; Cho, Jae Young ; Kim, Kyung Sup ; Lee, Su Jae ; Lee, Ki Hoo ; Choi, Kang-Yell. / Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells. In: Cellular Signalling. 2004 ; Vol. 16, No. 11. pp. 1309-1317.
@article{6912c357494e4004ad10de1d584ade3b,
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 Kang-Yell Choi",
year = "2004",
month = "11",
day = "1",
doi = "10.1016/j.cellsig.2004.04.004",
language = "English",
volume = "16",
pages = "1309--1317",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "11",

}

Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells. / Kim, Sung Eun; Cho, Jae Young; Kim, Kyung Sup; Lee, Su Jae; Lee, Ki Hoo; Choi, Kang-Yell.

In: Cellular Signalling, Vol. 16, No. 11, 01.11.2004, p. 1309-1317.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Drosophila PI3 kinase and Akt involved in insulin-stimulated proliferation and ERK pathway activation in Schneider cells

AU - Kim, Sung Eun

AU - Cho, Jae Young

AU - Kim, Kyung Sup

AU - Lee, Su Jae

AU - Lee, Ki Hoo

AU - Choi, Kang-Yell

PY - 2004/11/1

Y1 - 2004/11/1

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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=4444347661&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4444347661&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2004.04.004

DO - 10.1016/j.cellsig.2004.04.004

M3 - Article

VL - 16

SP - 1309

EP - 1317

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 11

ER -