Research Paper Volume 11, Issue 18 pp 7817—7829
PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling
Figure 5. The protein phosphorylation of stathmin and STATs signaling expressed in K562 and K562/G01 cells after PRL-3-silencing. (A) Stathmin, the four stathmin-serine sites, and β-actin expression were detected by western blot. (B–E) Quantification of stathmin-phospho (Ser16, Ser25, Ser38, and Ser63) were normalized to stathmin. (F) STAT3, p-STAT3, STAT5, p-STAT5 and β-actin expression were detected by western blot. (G–J) Quantification of p-STAT3 and p-STAT5 were normalized to STAT3 and STAT5, respectively. (*P<0.05, **P<0.01, vs. NC group).