期刊
GROWTH FACTORS
卷 26, 期 2, 页码 104-116出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/08977190802066655
关键词
mouse embryonic stem cell; TGF-alpha; PI3-K/Akt; p44/42 MAPKs; notch
This study examined the mechanisms by which transforming growth factor (TGF)-alpha regulates proliferation of mouse embryonic stem (ES) cells. TGF-alpha increased [H-3] thymidine and BrdU incorporation in a time- (0-72h) and dose-dependent (0-10ng/ml) manner. TGF-alpha stimulated the phosphorylation of Akt, mammalian target of rapamycin (mTOR), p70S6K1 and p44/42 mitogen-activated protein kinases (MAPKs). TGF-alpha also increased the protein levels of Notch, Notch intracellular domain, Hes-1 and Wnt1. However, TGF--induced DNA synthesis was blocked by inhibition of Akt, mTOR, p44/42 MAPKs and Notch. TGF-alpha increased the gene expression of c-jun, c-myc and c-fos. Moreover, TGF-alpha increased cyclin D/CDK 4 and cyclin E/CDK 2 levels, while decreasing p21(cip1/waf1) and p27(kip1), which were blocked by the inhibition of Akt, mTOR and Notch. In conclusion, TGF-alpha regulated DNA synthesis of mouse ES cells via PI3-K/Akt, p44/42 MAPKs and Notch/Wnt pathways.
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