Fig. 1.
Fig. 1. Induction of apoptosis by proteasome inhibition in CLL patient isolates. (A) DNA fragmentation analysis. Cells from a representative glucocorticoid-sensitive patient (see Table 1) were preincubated in the presence of 25 μmol/L zAPFcmk or 200 μmol/L zVADfmk for 1 hour and then treated with 10 μmol/L MG132, and DNA fragmentation was measured at 16 hours by PI staining and FACS analysis. (B) Surface phosphatidylserine exposure. Cells were incubated in absence or presence of 10 μmol/L methylprednisolone or 10 μmol/L MG132 with or without 200 μmol/L zVADfmk, and surface PS exposure was quantitated by staining with annexin-FITC and measured by FACS analysis. Results characteristic of three independent experiments with different patient isolates.

Induction of apoptosis by proteasome inhibition in CLL patient isolates. (A) DNA fragmentation analysis. Cells from a representative glucocorticoid-sensitive patient (see Table 1) were preincubated in the presence of 25 μmol/L zAPFcmk or 200 μmol/L zVADfmk for 1 hour and then treated with 10 μmol/L MG132, and DNA fragmentation was measured at 16 hours by PI staining and FACS analysis. (B) Surface phosphatidylserine exposure. Cells were incubated in absence or presence of 10 μmol/L methylprednisolone or 10 μmol/L MG132 with or without 200 μmol/L zVADfmk, and surface PS exposure was quantitated by staining with annexin-FITC and measured by FACS analysis. Results characteristic of three independent experiments with different patient isolates.

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