Figure 4
Figure 4. Aberrant signaling is required for PAX5 deregulation in t(8;21) AML. (A) Schematic diagram showing chronic AKT, JNK, JAK/STAT, and MAP kinase signaling in t(8;21) AML downstream of an activating mutation (indicated by a star) in a tyrosine kinase (growth factor) receptor or activated rat sarcoma (RAS) signaling. The circles indicate the signaling components targeted by small-molecule inhibitors. (B) Table listing the signaling components targeted, small-molecule inhibitors used, and the effect of the inhibitors on PAX5 expression in Kasumi-1 cells. For detailed data, see supplemental Figure 4A. (C-F) Quantitative reverse transcription PCR experiment measuring expression of PAX5, INK4/ARF, TBP, and RPL13A, respectively, after simultaneous treatment with JNK, MEK, and p38 inhibitors. Each bar graph is representative of 3 independent experiments. The error bars represent the variability in qPCR measurements.

Aberrant signaling is required for PAX5 deregulation in t(8;21) AML. (A) Schematic diagram showing chronic AKT, JNK, JAK/STAT, and MAP kinase signaling in t(8;21) AML downstream of an activating mutation (indicated by a star) in a tyrosine kinase (growth factor) receptor or activated rat sarcoma (RAS) signaling. The circles indicate the signaling components targeted by small-molecule inhibitors. (B) Table listing the signaling components targeted, small-molecule inhibitors used, and the effect of the inhibitors on PAX5 expression in Kasumi-1 cells. For detailed data, see supplemental Figure 4A. (C-F) Quantitative reverse transcription PCR experiment measuring expression of PAX5, INK4/ARF, TBP, and RPL13A, respectively, after simultaneous treatment with JNK, MEK, and p38 inhibitors. Each bar graph is representative of 3 independent experiments. The error bars represent the variability in qPCR measurements.

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