Figure 4
Downstream signaling induced by anti-Ig or DC-SIGN is ablated by kinase inhibitors. PhosFlow data analysis to examine phosphorylation of PLCγ2 and ERK in FL cells. Cells were pretreated with H2O2 to inhibit phosphatases before stimulation with either crosslinked DC-SIGN (xDC-SIGN) or soluble anti-Ig. (A) Cytobank software (representative heat map traces shown) was used to measure phosphorylation of PLCγ2 and ERK for each treatment at each time point. (B) Fold-change analysis was used to chart the level of phosphorylation over time in 13 samples tested. (C) PhosFlow was used to measure the impact of the SYK inhibitor tamatinib or BTK inhibitor ibrutinib on phosphorylation of PLCγ2 and ERK. Analysis of data for 9 samples (6 for SYK and 3 for BTK) was compiled (GraphPad Prism) (Student t test; ****P < .0001).

Downstream signaling induced by anti-Ig or DC-SIGN is ablated by kinase inhibitors. PhosFlow data analysis to examine phosphorylation of PLCγ2 and ERK in FL cells. Cells were pretreated with H2O2 to inhibit phosphatases before stimulation with either crosslinked DC-SIGN (xDC-SIGN) or soluble anti-Ig. (A) Cytobank software (representative heat map traces shown) was used to measure phosphorylation of PLCγ2 and ERK for each treatment at each time point. (B) Fold-change analysis was used to chart the level of phosphorylation over time in 13 samples tested. (C) PhosFlow was used to measure the impact of the SYK inhibitor tamatinib or BTK inhibitor ibrutinib on phosphorylation of PLCγ2 and ERK. Analysis of data for 9 samples (6 for SYK and 3 for BTK) was compiled (GraphPad Prism) (Student t test; ****P < .0001).

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