Figure 1.
Figure 1. Effect of imatinib on BCR-ABL kinase activity and growth of cells expressing BCR-ABL kinase domain mutants. (A) TF-1 cells expressing BCR-ABL kinase domain mutations and wild-type BCR-ABL were exposed to imatinib (0 to 10 μM) for 4 hours. Whole-cell lysates were analyzed by Western blotting using antiphosphotyrosine (PY) and anti-abl (ABL) antibodies. WB indicates Western blot. (B) TF-1 cells expressing mutant BCR-ABL genes were cultured in the presence of imatinib (0 to 10 μM) for 3 days. Viable cells were quantified using an MTS assay. The resulting optical density (OD) values were expressed as percentage of controls cultured simultaneously without imatinib. □ indicates wild type; ▿, E373G; ▴, M237I; ▾, L248V; , D276G; ⬡, G321E; and ▪, Y353H. Each data point represents the mean of 3 experiments (except wild-type [n = 2]), with each experiment based on 3 replicates. Curve fitting was performed using GraphPad Prism software.

Effect of imatinib on BCR-ABL kinase activity and growth of cells expressing BCR-ABL kinase domain mutants. (A) TF-1 cells expressing BCR-ABL kinase domain mutations and wild-type BCR-ABL were exposed to imatinib (0 to 10 μM) for 4 hours. Whole-cell lysates were analyzed by Western blotting using antiphosphotyrosine (PY) and anti-abl (ABL) antibodies. WB indicates Western blot. (B) TF-1 cells expressing mutant BCR-ABL genes were cultured in the presence of imatinib (0 to 10 μM) for 3 days. Viable cells were quantified using an MTS assay. The resulting optical density (OD) values were expressed as percentage of controls cultured simultaneously without imatinib. □ indicates wild type; ▿, E373G; ▴, M237I; ▾, L248V; , D276G; ⬡, G321E; and ▪, Y353H. Each data point represents the mean of 3 experiments (except wild-type [n = 2]), with each experiment based on 3 replicates. Curve fitting was performed using GraphPad Prism software.

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