Figure 1.
Figure 1. Constitutive STAT5 activation in AMKL cell lines and inhibitory effect of the JAK inhibitor I on CHRF-288-11 cells. (A) Constitutive phosphorylation of STAT5 in AMKL cell lines. (B) Dose-dependent growth inhibition of CHRF-288-11 and HEL cells, but not K562 cells, with increasing concentrations of JAK inhibitor I. The MTT assay was performed at 72 hours. Mean value plus or minus SD of experiments performed in triplicate is represented. For each individual cell line, growth in the presence of an increasing amount of inhibitor was normalized to the vehicle control (0 nM) growth. (C) Inhibition of STAT5 phosphorylation by JAK inhibitor I in CHRF-288-11 cells but not in K562 cells. (D) Induction of apoptosis (annexin V+/PI- cells, bottom right quadrant) and cell death (annexin V+/PI+ cells, top right quadrant) in CHRF-288-11 cells treated by JAK inhibitor I, at 72 hours. Percentage of total population is indicated.

Constitutive STAT5 activation in AMKL cell lines and inhibitory effect of the JAK inhibitor I on CHRF-288-11 cells. (A) Constitutive phosphorylation of STAT5 in AMKL cell lines. (B) Dose-dependent growth inhibition of CHRF-288-11 and HEL cells, but not K562 cells, with increasing concentrations of JAK inhibitor I. The MTT assay was performed at 72 hours. Mean value plus or minus SD of experiments performed in triplicate is represented. For each individual cell line, growth in the presence of an increasing amount of inhibitor was normalized to the vehicle control (0 nM) growth. (C) Inhibition of STAT5 phosphorylation by JAK inhibitor I in CHRF-288-11 cells but not in K562 cells. (D) Induction of apoptosis (annexin V+/PI- cells, bottom right quadrant) and cell death (annexin V+/PI+ cells, top right quadrant) in CHRF-288-11 cells treated by JAK inhibitor I, at 72 hours. Percentage of total population is indicated.

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