Figure 3
Figure 3. Dose- and time-dependent effects of MCL-1 antisense oligonucleotides on neoplastic mast cells. (A-B) Western blot analysis of MCL-1 expression in HMC-1.1 cells (A) and HMC-1.2 cells (B) after exposure to various concentrations of MCL-1 antisense oligonucleotides (Antisense) (50-250 nM) or control medium (Control) for 12 hours. β-Actin served as loading control. (C-D) Time-dependent effects of MCL-1 antisense oligonucleotides (Antisense) (250 nM) and a scramble Control (250 nM) on expression of the MCL-1 protein in HMC-1.1 cells (C) and HMC-1.2 cells (D). MCL-1 expression was determined by Western blotting, with β-actin serving as a loading control. (C-D, lower) Time-dependent effects of the MCL-1 antisense oligonucleotides (250 nM) and of the scramble Control (250 nM) on cell viability (ie, percentage) of apoptotic HMC-1.1 cells (C) and HMC-1.2 cells (D). Results represent the mean ± SD from 3 independent experiments.

Dose- and time-dependent effects of MCL-1 antisense oligonucleotides on neoplastic mast cells. (A-B) Western blot analysis of MCL-1 expression in HMC-1.1 cells (A) and HMC-1.2 cells (B) after exposure to various concentrations of MCL-1 antisense oligonucleotides (Antisense) (50-250 nM) or control medium (Control) for 12 hours. β-Actin served as loading control. (C-D) Time-dependent effects of MCL-1 antisense oligonucleotides (Antisense) (250 nM) and a scramble Control (250 nM) on expression of the MCL-1 protein in HMC-1.1 cells (C) and HMC-1.2 cells (D). MCL-1 expression was determined by Western blotting, with β-actin serving as a loading control. (C-D, lower) Time-dependent effects of the MCL-1 antisense oligonucleotides (250 nM) and of the scramble Control (250 nM) on cell viability (ie, percentage) of apoptotic HMC-1.1 cells (C) and HMC-1.2 cells (D). Results represent the mean ± SD from 3 independent experiments.

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