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

First Author  Seoane J Year  2004
Journal  Cell Volume  117
Issue  2 Pages  211-23
PubMed ID  15084259 Mgi Jnum  J:235266
Mgi Id  MGI:5795826 Doi  10.1016/s0092-8674(04)00298-3
Citation  Seoane J, et al. (2004) Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation. Cell 117(2):211-23
abstractText  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.
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