Open Access Highly Accessed Research article

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 Terragni1, Julie R Graham1, Kenneth W Adams12, Michael E Schaffer13, John W Tullai1 and Geoffrey M Cooper1*

  • * Corresponding author: Geoffrey M Cooper gmcooper@bu.edu

  • † Equal contributors

Author Affiliations

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

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

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

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

Published: 28 January 2008

Additional files

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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