Fig. 5.

Plerixafor induces phosphorylation of receptor tyrosine kinases. a Phospho-RTK arrays were probed with whole cell lysates of CXCR4-low A673 and CXCR4-high TC-32 cells that were treated with 1 μM plerixafor or DMSO vehicle for 1 h. b RTKs activated by plerixafor. Mean pixel densities of duplicate RTK capture spots were measured and normalized to mean pixel densities of control spots of respective membranes. RTKs phosphorylated in the presence of plerixafor (mean normalized pixel density above the mean of all RTKs) were defined as active and considered for analysis. Fold changes (fc) of normalized mean pixel densities in plerixafor-treated (grey bars) compared to control cells (black bars) were calculated and RTKs with an activation fold change greater than the mean (Z-score (z) of fold change > 0) were defined as plerixafor-activated. The full data set is available in Additional file 2