Activation of PI3K/Akt pathway by CD133-p85 interaction promotes tumorigenic capacity of glioma stem cells
出版年份 2013 全文链接
标题
Activation of PI3K/Akt pathway by CD133-p85 interaction promotes tumorigenic capacity of glioma stem cells
作者
关键词
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出版物
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 110, Issue 17, Pages 6829-6834
出版商
Proceedings of the National Academy of Sciences
发表日期
2013-04-09
DOI
10.1073/pnas.1217002110
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- CD133 expression is associated with poor outcome in neuroblastoma via chemoresistance mediated by the AKT pathway
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- Lipid rafts play an important role for maintenance of embryonic stem cell self-renewal
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- The Stem Cell Marker CD133 (Prominin-1) is Phosphorylated on Cytoplasmic Tyrosine-828 and Tyrosine-852 by Src and Fyn Tyrosine Kinases
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- Somatic Mutations in p85α Promote Tumorigenesis through Class IA PI3K Activation
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- Comprehensive genomic characterization defines human glioblastoma genes and core pathways
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- Glioma Formation, Cancer Stem Cells, and Akt Signaling
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- Brain Cancer Stem Cells Display Preferential Sensitivity to Akt Inhibition
- (2008) Christine E. Eyler et al. STEM CELLS
- CD133 negative glioma cells form tumors in nude rats and give rise to CD133 positive cells
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