Fig. 5.
Fig. 5. Effect of tyrosine kinase inhibitors on tyrosine phosphorylation, PARP cleavage, and survival of K562 and K562-R cells. / (A) K562 (left) and K562-R (right) cells were treated with 1 μM STI571, 10 μM PP2, or 1 μM PD180970 for 24 hours before PARP cleavage was monitored by immunoblotting. Intact and cleaved PARP are depicted. (B) K562 and K562-R cells were treated with PD180970 (at the concentration indicated) for 24 hours in a 96-well plate before survival was quantitated by MTT assay (described in “Materials and methods”) and compared to control (untreated) cells. Control cell survival was set at 100%. The results represent the average ± SEM of 4 determinations. (C) K562 and K562-R cells were incubated with the indicated concentration of PP2 for 48 hours in a 96-well plate before cell survival was estimated by MTT assay. Each data point represents the average ± SEM of 4 determinations. Untreated (control) cell survival was set at 100%.

Effect of tyrosine kinase inhibitors on tyrosine phosphorylation, PARP cleavage, and survival of K562 and K562-R cells.

(A) K562 (left) and K562-R (right) cells were treated with 1 μM STI571, 10 μM PP2, or 1 μM PD180970 for 24 hours before PARP cleavage was monitored by immunoblotting. Intact and cleaved PARP are depicted. (B) K562 and K562-R cells were treated with PD180970 (at the concentration indicated) for 24 hours in a 96-well plate before survival was quantitated by MTT assay (described in “Materials and methods”) and compared to control (untreated) cells. Control cell survival was set at 100%. The results represent the average ± SEM of 4 determinations. (C) K562 and K562-R cells were incubated with the indicated concentration of PP2 for 48 hours in a 96-well plate before cell survival was estimated by MTT assay. Each data point represents the average ± SEM of 4 determinations. Untreated (control) cell survival was set at 100%.

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