Skip to main content
. Author manuscript; available in PMC: 2017 Mar 3.
Published in final edited form as: Nature. 2007 Nov 29;450(7170):731–735. doi: 10.1038/nature06305

Figure 1. Specific and severe defect in Raf–MEK–ERK activation in Cnb1-deficient thymocytes.

Figure 1

a, Expression of CD4 and CD8 on Cnb1-deficient and control thymocytes. The numbers in the corners of the panels represent the percentage of cells in each quadrant. b, Immunoblot analysis of phosphorylated and total proteins in Cnb1-deficient and control double-positive thymocytes after CD3ε crosslinking. GSK, glycogen synthase kinase; PKC, protein kinase C; PKD, protein kinase D. c, Immunoblot analysis of phosphorylated ERK1/2 in Cnb1-deficient and control double-positive thymocytes after CD3ε crosslinking. d, Immunoblot analysis of Egr1 induction in double-positive thymocytes from Cnb1-deficient and control littermates. Brg1 shows equal loading. e, Immunoblot analysis of phosphorylated MEK1/2 in Cnb1-deficient and control double-positive thymocytes after CD3ε crosslinking. f, Raf-B kinase activity in Cnb1-deficient and control double-positive thymocytes after CD3ε crosslinking. IP, immunoprecipitation; IB, immunoblotting.