期刊
ONCOGENE
卷 24, 期 37, 页码 5722-5730出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1208925
关键词
TGF-beta; CNS cancer; glioblastoma; ELF; Smad
资金
- NIDDK NIH HHS [R01 DK58637] Funding Source: Medline
Transforming growth factor beta (TGF-beta) signaling leads to a number of biological end points involving cell growth, differentiation, and morphogenesis. Typically, the cellular effect accompanies an induction of mesodermal cell fate and inhibition of neural cell differentiation. However, during pathological conditions, these defined effects of TGF-beta can be reversed; for example, the growth-inhibitory effect is replaced with its tumor promoting ability. A multitude of factors and cross-signaling pathways have been reported to be involved in modulating the dual effects of TGF-beta. In this review, we focus on the potential role of TGF-beta signal transduction during development of neural progenitor cells and its relation to glioblastoma development from neural stem cells.
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