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 | |
| Publication status | Published - 2004 Nov 1 |
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All Science Journal Classification (ASJC) codes
- Cell Biology
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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 journal › Article
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.
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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 -