期刊
CELL
卷 117, 期 2, 页码 211-223出版社
CELL PRESS
DOI: 10.1016/S0092-8674(04)00298-3
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资金
- NCI NIH HHS [CA34610] Funding Source: Medline
- NINDS NIH HHS [NS44819] Funding Source: Medline
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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