Phosphatidylinositol 3-kinase signaling in proliferating cells maintains an anti-apoptotic transcriptional program mediated by inhibition of FOXO and non-canonical activation of NFκB transcription factors

Jolyon Terragni^*¹ , Julie R Graham^*¹ , Kenneth W Adams¹^,2 , Michael E Schaffer¹^,3 , John W Tullai¹ and Geoffrey M Cooper¹

¹Department of Biology, Boston University, Boston MA 02215, USA

²Current Address: Alzheimer's Disease Research Center, Massachusetts General Hospital, Charlestown, MA 02129, USA

³Current Address: Pfizer, Inc., Research Technology Center, 620 Memorial Drive, Cambridge, MA 02139, USA

author email corresponding author email* Contributed equally

BMC Cell Biology 2008, 9:6doi:10.1186/1471-2121-9-6


Published:	28 January 2008

Additional file 1:

Expression changes arising after 2, 4, and 8 hours of PI 3-kinase inhibition

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Additional file 2:

Effects of LY294002 and wortmannin on gene expression

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Additional file 3:

TRANSFAC matrices tested for over-representation in the genes that were differentially expressed after 2 and 4 hours of PI 3-kinase inhibition

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Additional file 4:

Predicted FOXO and NFκB binding sites in the genes that were either up- or down-regulated after PI 3-kinase inhibition

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