Figure 3
Figure 3. RAC1 is the main STAT3 activator in TEL-AML1 leukemia. (A-B) Western blot analysis of GTP-Rac1 pull-downs and total Rac1 from mouse HPC (A), 72 hours after transduction with MSCV T/A or MSCV CD2, and Reh cells (B), 5 days after transduction with control scramble or shTA shRNA. Numbers represent densitometric quantitation of GTP-Rac1 normalized to total RAC1 (A), and GTP-RAC1, and total RAC1 normalized to HSP90 (B). (C) Flow cytometric analysis of p-Y705 STAT3 in Reh, 5 hours after treatment with 50 μM (MFI = 12.99) and 100 μM (MFI = 11.66) NSC23766 or dimethylsulfoxide (MFI = 15.57). (D) Percentage of Reh and At-2 apoptotic Annexin V+PI- cells 24 hours after dimethylsulfoxide or 50 µM NSC23766 treatment. Data are representative of 2 (B) and 3 (A, C, and D) independent experiments. *P < .05, **P < .01, ***P < .005 compared with control (Student unpaired t test). GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

RAC1 is the main STAT3 activator in TEL-AML1 leukemia. (A-B) Western blot analysis of GTP-Rac1 pull-downs and total Rac1 from mouse HPC (A), 72 hours after transduction with MSCV T/A or MSCV CD2, and Reh cells (B), 5 days after transduction with control scramble or shTA shRNA. Numbers represent densitometric quantitation of GTP-Rac1 normalized to total RAC1 (A), and GTP-RAC1, and total RAC1 normalized to HSP90 (B). (C) Flow cytometric analysis of p-Y705 STAT3 in Reh, 5 hours after treatment with 50 μM (MFI = 12.99) and 100 μM (MFI = 11.66) NSC23766 or dimethylsulfoxide (MFI = 15.57). (D) Percentage of Reh and At-2 apoptotic Annexin V+PI- cells 24 hours after dimethylsulfoxide or 50 µM NSC23766 treatment. Data are representative of 2 (B) and 3 (A, C, and D) independent experiments. *P < .05, **P < .01, ***P < .005 compared with control (Student unpaired t test). GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

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