Fig. 1: JAK2 ATP-competitive inhibitors treatment leads to paradox JAK2 hyperphosphorylation. | Leukemia

Fig. 1: JAK2 ATP-competitive inhibitors treatment leads to paradox JAK2 hyperphosphorylation.

From: Ruxolitinib mediated paradoxical JAK2 hyperphosphorylation is due to the protection of activation loop tyrosines from phosphatases

Fig. 1

Ba/F3 cells expressing the JAK2-V617F and JAK2-WT were treated with the indicated concentration of the ruxolitinib (A) fedratinib (B) and lestaurtinib (C) for 3 h, and lysates were prepared and subjected to western blotting for the pJAK2, JAK2, pSTAT5 and STAT5. Ba/F3 cells expressing the JAK1-V658F and JAK1-WT were treated for 3.5 h with ruxolitinib, and lysates were analyzed for activation of JAK1 and STAT3 (D). Ba/F3 cells stably expressing the CSF3R-T618I and CSF3R-WT treated with indicated concentrations of ruxolitinib (E) and G-CSF (F) for 3 h, and lysates were subjected to western blotting for the pTYK2, TYK2, pSTAT3, STAT3, pSTAT5 and STAT5. Ba/F3 cells expressing the JAK3-WT were treated with indicated concentrations of ruxolitinib in the presence of interleukin-2 (IL-2), and lysates were subjected to western blotting for the pJAK3, JAK3, pSTAT3 and STAT3 (G).

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