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Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation.

Cell | Apr 16, 2004

http://www.ncbi.nlm.nih.gov/pubmed/15084259

FoxO Forkhead transcription factors are shown here to act as signal transducers at the confluence of Smad, PI3K, and FoxG1 pathways. Smad proteins activated by TGF-beta form a complex with FoxO proteins to turn on the growth inhibitory gene p21Cip1. This process is negatively controlled by the PI3K pathway, a known inhibitor of FoxO localization in the nucleus, and by the telencephalic development factor FoxG1, which we show binds to FoxO-Smad complexes and blocks p21Cip1 expression. We suggest that the activity of this network confers resistance to TGF-beta-mediated cytostasis during the development of the telencephalic neuroepithelium and in glioblastoma brain tumor cells.

Pubmed ID: 15084259 RIS Download

Mesh terms: Animals | Brain Neoplasms | Cell Division | Cell Line, Tumor | Cell Transformation, Neoplastic | Cyclin-Dependent Kinase Inhibitor p21 | Cyclins | DNA-Binding Proteins | Fetus | Forkhead Transcription Factors | Gene Expression Regulation, Developmental | Glioblastoma | Humans | Mice | Mice, Inbred C57BL | Mice, Knockout | Phosphatidylinositol 3-Kinases | Protein Binding | Signal Transduction | Smad Proteins | Stem Cells | Telencephalon | Trans-Activators | Transcription Factors | Transforming Growth Factor beta

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Associated grants

  • Agency: NCI NIH HHS, Id: CA34610
  • Agency: NINDS NIH HHS, Id: NS44819

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