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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Cancer Res. 2009 Jan 20;69(3):810–818. doi: 10.1158/0008-5472.CAN-08-2473

Figure 5.

Figure 5

CDK6 operates downstream of Akt kinase. A, Comparison of tumor susceptibility between WT; Akt (n=21), Het;Akt (n=17), and KO;Akt (n=15) mice. B, Western blot analysis of thymocyte lysates derived from 4-week old WT or KO mice (left panel) or WT (lane 1) or WT;Akt (lane 2, pretumor) or 4-month old KO;Akt (lane 3) mice or WT;Akt (tumor cells, lane 4, right panel). Immunoblots were probed with different antibodies as indicated. Actin was used as an internal control to ensure equal loading. Anti-HA was used to detect transgene MyrAkt and distinguish it from endogenous Akt. C, On the left, the MyrAkt transgene failed to promote β-selection in the absence of CDK6. DN thymocytes from 4-week old WT;Akt and KO;Akt mice stained with the ‘cocktail’ of lineage-specific antibodies and anti-CD44 and anti-CD25. Lineage-positive cells were electronically ‘gated out’ and CD44-versus-CD25 profiles of the lineage-negative compartments are presented. Numbers in quadrants indicate the percentage of cells in each subset stained with CD44 and CD25. The bar graph (right panel) summarizes percentage of each subset from separate (n=3 for WT;Akt, n=4 for KO;Akt) experiments. Data are expressed as mean ± S.E. *, p < 0.05, significantly different from the control levels. D, Comparisons of flow cytometric analysis of CD44 (left panel) or CD25 (right panel) expression in some compartments from WT;Akt and KO;Akt.