Figure 3
Modulation of ERK1/2 and p38 MAPK pathways. (A) Daudi cells were treated with 133nM each of rituximab, epratuzumab, and veltuzumab and 10nM each of 20-20, 22-20, and 20-22 separately for 24 hours. Cells were immunoblotted and probed with phospho-specific antibodies as well as with antibodies to ERK1/2, p38, and β-actin. Bar diagrams show the relative intensity of phospho-ERK or phospho-p38 induced by each agent, as determined by densitometry analysis of the results from 2 or more independent experiments. (B) Phospho-ERK1/2 induced by 20-20, 22-20, and 20-22 or rituximab at 10nM measured at various time points within the first 24 hours. (C) Up-regulation of phospho-ERK1/2 by crosslinking rituximab and veltuzumab with GAH (10 μg/mL).

Modulation of ERK1/2 and p38 MAPK pathways. (A) Daudi cells were treated with 133nM each of rituximab, epratuzumab, and veltuzumab and 10nM each of 20-20, 22-20, and 20-22 separately for 24 hours. Cells were immunoblotted and probed with phospho-specific antibodies as well as with antibodies to ERK1/2, p38, and β-actin. Bar diagrams show the relative intensity of phospho-ERK or phospho-p38 induced by each agent, as determined by densitometry analysis of the results from 2 or more independent experiments. (B) Phospho-ERK1/2 induced by 20-20, 22-20, and 20-22 or rituximab at 10nM measured at various time points within the first 24 hours. (C) Up-regulation of phospho-ERK1/2 by crosslinking rituximab and veltuzumab with GAH (10 μg/mL).

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