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. 2015 Apr 9;20(1):736–746. doi: 10.2119/molmed.2014.00146

Figure 4.

Figure 4

G-CSFRIV mediates aberrant activation of the Stat3, Stat5, ERK1/2 and AKT signaling pathways. CD34+ HSPCs were transduced with a lentiviral vector encoding for either G-CSFRI or G-CSFRIV sequences. Unsorted serum-starved cells (1 × 105) were stimulated with 100 ng/mL G-CSF for sequential time points from 0 to 150 min and signaling pathway analysis was performed. GFP expression was used to distinguish G-CSFR overexpressing and nontransduced cells. Levels of phosphorylated proteins at different time points were compared with the respective phosphorylated protein level detected without stimulation. Graph displays MFI of G-CSF–induced phosphorylated Stat3 (A), Stat5 (B), ERK1/2 (C) and AKT (D) in G-CSFRI+, G-CSFRIV+, G-CSFRI− and G-CSFRIV− HSPCs. Data shown are mean ± SD of six independent experiments. Statistically significant differences were calculated using a two-tailed Student t test and are shown with asterisks (*p < 0.05 and **p < 0.01). G-CSFRI−, G-CSFRI nontransduced; G-CSFRIV−, G-CSFRIV nontransduced.