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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.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Kim SE,Cho JY,Kim KS,Lee SJ,Lee KH,Choi KY

doi

10.1016/j.cellsig.2004.04.004

subject

Has Abstract

pub_date

2004-11-01 00:00:00

pages

1309-17

issue

11

eissn

0898-6568

issn

1873-3913

pii

S0898656804000609

journal_volume

16

pub_type

杂志文章

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