American Society of Hematology

Figure 2.

$Figure 2. Role of NF-κB in KIT D816V–dependent expression of CCL2. (A) Effects of piceatannol (200 µM), PD98059 (50 µM), LY294002 (20 µM), or BEZ253 (1 µM) on expression of CCL2 in HMC-1 cells. (B) HMC-1 cells were treated with TPCA-1 (20 µM), and the effect on NF-κB signaling was determined by immunoblotting with antibodies against NF-κB in cytoplasmic and nuclear fractions as well as IκB and phosphorylated IκB (pIκB) in whole-cell lysates. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), histone H3, and β-actin served as the respective loading controls. (C-D) Effect of TPCA-1 treatment (C) as indicated or (D) of RNAi-mediated knockdown of NF-κB1 compared with an NTC on expression of CCL2 in HMC-1 cells. (E) TF-1 cells were transduced with CO, WT KIT, or KIT D816V, and NF-κB signaling was analyzed as described above. Results represent the mean ± SD of at least 3 independent experiments. **P < .01, ***P < .001.$

Role of NF-κB in KIT D816V–dependent expression of CCL2. (A) Effects of piceatannol (200 µM), PD98059 (50 µM), LY294002 (20 µM), or BEZ253 (1 µM) on expression of CCL2 in HMC-1 cells. (B) HMC-1 cells were treated with TPCA-1 (20 µM), and the effect on NF-κB signaling was determined by immunoblotting with antibodies against NF-κB in cytoplasmic and nuclear fractions as well as IκB and phosphorylated IκB (pIκB) in whole-cell lysates. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), histone H3, and β-actin served as the respective loading controls. (C-D) Effect of TPCA-1 treatment (C) as indicated or (D) of RNAi-mediated knockdown of NF-κB1 compared with an NTC on expression of CCL2 in HMC-1 cells. (E) TF-1 cells were transduced with CO, WT KIT, or KIT D816V, and NF-κB signaling was analyzed as described above. Results represent the mean ± SD of at least 3 independent experiments. **P < .01, ***P < .001.

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