The conserved PI3′K/PTEN/Akt signaling pathway regulates both cell size and survival in Drosophila

被引:0
|
作者
Sam E Scanga
Laurent Ruel
Richard C Binari
Brian Snow
Vuk Stambolic
Denis Bouchard
Malte Peters
Batista Calvieri
Tak W Mak
James R Woodgett
Armen S Manoukian
机构
[1] Ontario Cancer Institute,Department of Medical Biophysics, Division of Cell and Molecular Biology
[2] University Health Network,Department of Medical Biophysics, Division of Experimental Therapeutics
[3] Princess Margaret Hospital,undefined
[4] University of Toronto,undefined
[5] 610 University Avenue,undefined
[6] Ontario Cancer Institute,undefined
[7] University Health Network,undefined
[8] Princess Margaret Hospital,undefined
[9] University of Toronto,undefined
[10] 610 University Avenue,undefined
[11] Amgen Research Institute,undefined
[12] 620 University Avenue,undefined
[13] Electron Microscopy Unit,undefined
[14] Medical Sciences Building,undefined
[15] Faculty of Medicine,undefined
[16] University of Toronto,undefined
来源
Oncogene | 2000年 / 19卷
关键词
PKB; PI3K; PTEN; cell size; cell survival;
D O I
暂无
中图分类号
学科分类号
摘要
Akt (or PKB) is an oncogene involved in the regulation of cell survival. Akt is regulated by phosphatidylinositol 3-OH kinase (PI3′K) signaling and has shown to be hyperactivated through the loss of the PTEN tumor suppressor. In Drosophila, insulin signaling as studied using the Drosophila IRS-4 homolog (Chico) has been shown to be a crucial regulator of cell size. We have studied Drosophila Akt (Dakt1) and have shown that it is also involved in the regulation of cell size. Furthermore we have performed genetic epistasis tests to demonstrate that in Drosophila, PI3′K, PTEN and Akt comprise a signaling cassette that is utilized during multiple stages of development. In addition, we show that this signaling cassette is also involved in the regulation of cell survival during embryogenesis. This study therefore establishes the evolutionary conservation of this signaling pathway in Drosophila.
引用
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页码:3971 / 3977
页数:6
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