Figure 2
Figure 2. AEB071 attenuates BCR-dependent activation. (A-B) CD19+ cells from CLL patients (N = 8) were treated with AEB071 (2 μM) and stimulated with immobilized anti-IgM for 24 hours. ERK phosphorylation at Thr202/Tyr204, AKT phosphorylation at Ser473, GSK3-β phosphorylation at Ser9, and IκBα phosphorylation was assessed by immunoblot. Results from 2 patients are presented; black line indicates cropped regions wherein only relevant bands are shown. Band quantification is represented as fold change from unstimulated control (mean ± standard deviation [SD]). (C) CD19+ cells from CLL patients (N = 11) were stimulated with immobilized anti-IgM in presence or absence of AEB071 (2 μM) for 24 hours and cytotoxicity was measured by annexin/PI staining. Dark lines represent averages.

AEB071 attenuates BCR-dependent activation. (A-B) CD19+ cells from CLL patients (N = 8) were treated with AEB071 (2 μM) and stimulated with immobilized anti-IgM for 24 hours. ERK phosphorylation at Thr202/Tyr204, AKT phosphorylation at Ser473, GSK3-β phosphorylation at Ser9, and IκBα phosphorylation was assessed by immunoblot. Results from 2 patients are presented; black line indicates cropped regions wherein only relevant bands are shown. Band quantification is represented as fold change from unstimulated control (mean ± standard deviation [SD]). (C) CD19+ cells from CLL patients (N = 11) were stimulated with immobilized anti-IgM in presence or absence of AEB071 (2 μM) for 24 hours and cytotoxicity was measured by annexin/PI staining. Dark lines represent averages.

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