Figure 5
Figure 5. Molecular characterization of IRF4−/−Vh11 CLL cells. (A) Splenic CLL cells were isolated from 5 IRF4−/−Vh11 mice via negative selection and lysed for western blot analysis with indicated antibodies. Splenic B cells from IRF4+/+Vh11(Vh11) and IRF4+/+ (B6) mice were also isolated and analyzed as controls. Additionally, splenic CLL cells from EµTcl1 transgenic mice were used as positive control for Tcl-1 expression. The numbers below each lane indicate the fold change in comparison with the control. The intensity of each protein was normalized initially to β-actin. (B) Total RNA was also extracted from the isolated cells. Real-time TaqMan polymerase chain reaction to detect expression of miR15a/16-1 was done using a kit from Applied Biosystems. The data were normalized to U6 spliceosomal RNA and were expressed as fold change in comparison with controls (IRF4+/+Vh11).

Molecular characterization of IRF4−/−Vh11 CLL cells. (A) Splenic CLL cells were isolated from 5 IRF4−/−Vh11 mice via negative selection and lysed for western blot analysis with indicated antibodies. Splenic B cells from IRF4+/+Vh11(Vh11) and IRF4+/+ (B6) mice were also isolated and analyzed as controls. Additionally, splenic CLL cells from EµTcl1 transgenic mice were used as positive control for Tcl-1 expression. The numbers below each lane indicate the fold change in comparison with the control. The intensity of each protein was normalized initially to β-actin. (B) Total RNA was also extracted from the isolated cells. Real-time TaqMan polymerase chain reaction to detect expression of miR15a/16-1 was done using a kit from Applied Biosystems. The data were normalized to U6 spliceosomal RNA and were expressed as fold change in comparison with controls (IRF4+/+Vh11).

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