Tumor Initiating Cells, Cell Cycle Control and Cancer Stem Cells
Tumor Initiating Cells, Cell Cycle Control and Cancer Stem Cells Tumor Initiating Cells, Cell Cycle Control and Cancer Stem Cells
Proliferation of Cyclin D1 −/− D2 −/− D3 −/− Cells Is Resistant to p16 INK4a but not p27 and Sensitive to CDK2 siRNA (over-expression of p16 - no effect) >>> In the absence of D cyclins pRb is phosphorylated by Cyclin-E-CDK2
Molecular Analyses of G1 Phase Progression in Cyclin D1 −/− D2 −/− D3 −/− Cells pRb and p107 are phosphorylated with a delayed kinetics and not to maximal level P27 is degraded faster in TKO, Perhaps it is phosphorylated more efficiently on Thr-187 by Cyclin E-CDK2 - but this is not shown. Cyclin E associated kinase activity increases in TKO E2F regulated genes are induced but not to maximal level
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- Page 42 and 43: Figure 8.15a The Biology of Cancer
- Page 44 and 45: Regulation of p27 localization AKT
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Molecular Analyses of G1 Phase Progression in Cyclin D1 −/− D2 −/− D3 −/− <strong><strong>Cell</strong>s</strong><br />
pRb <strong>and</strong> p107 are phosphorylated with a delayed kinetics<br />
<strong>and</strong> not to maximal level<br />
P27 is degraded faster in TKO,<br />
Perhaps it is phosphorylated more efficiently on Thr-187<br />
by Cyclin E-CDK2 - but this is not shown.<br />
Cyclin E associated kinase activity increases in TKO<br />
E2F regulated genes are induced but not to maximal level