Figure 5.
p.Ala119Thr CSF3R variants result in defective STAT activation, whereas p.Pro784Thr CSF3R variants show a trend toward increased STAT activation. Cells expressing p.Ala119Thr CSF3R (A-B), p.Pro784Thr CSF3R (C-D), or WT CSF3R (A-D) were serum and cytokine deprived for 2 hours and then stimulated with 10 ng/mL of G-CSF for the indicated times in minutes. Whole-cell lysates were immunoblotted with antibodies to phosphorylated STAT5 (pSTAT5), pSTAT3, and β-actin. Representative blots of 4 independent experiments for each CSF3R variant are shown. Densitometric analyses of the immunoblots were performed using ImageJ software. The data are presented as the ratios of pSTAT/β-actin. Error bars show the standard error. *P < .05.

p.Ala119Thr CSF3R variants result in defective STAT activation, whereas p.Pro784Thr CSF3R variants show a trend toward increased STAT activation. Cells expressing p.Ala119Thr CSF3R (A-B), p.Pro784Thr CSF3R (C-D), or WT CSF3R (A-D) were serum and cytokine deprived for 2 hours and then stimulated with 10 ng/mL of G-CSF for the indicated times in minutes. Whole-cell lysates were immunoblotted with antibodies to phosphorylated STAT5 (pSTAT5), pSTAT3, and β-actin. Representative blots of 4 independent experiments for each CSF3R variant are shown. Densitometric analyses of the immunoblots were performed using ImageJ software. The data are presented as the ratios of pSTAT/β-actin. Error bars show the standard error. *P < .05.

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