Fig. 6.
Fig. 6. Inhibition of CdA-induced apoptosis by BAPTA-AM and selective cross-resistance to thapsigargin. / (A) Cells were treated with 1 μM thapsigargin or 1 μM CdA for 12 hours, and DEVDase activity was quantitated as described in “Materials and methods.” CdA-induced caspase-3 activity was abrogated by preincubating the cells for 15 minutes in the presence of 50 μM BAPTA-AM, a cell-permeant Ca2+chelator. (B) Cells were treated with diluent alone, staurosporine (100 nM) for 6 hours, or anti-Fas mAb (250 ng/mL) for 3 hours. DNA fragmentation was assessed by propidium iodide staining and subsequent FACS analysis on the FL3 channel of a Becton Dickinson FACScan.

Inhibition of CdA-induced apoptosis by BAPTA-AM and selective cross-resistance to thapsigargin.

(A) Cells were treated with 1 μM thapsigargin or 1 μM CdA for 12 hours, and DEVDase activity was quantitated as described in “Materials and methods.” CdA-induced caspase-3 activity was abrogated by preincubating the cells for 15 minutes in the presence of 50 μM BAPTA-AM, a cell-permeant Ca2+chelator. (B) Cells were treated with diluent alone, staurosporine (100 nM) for 6 hours, or anti-Fas mAb (250 ng/mL) for 3 hours. DNA fragmentation was assessed by propidium iodide staining and subsequent FACS analysis on the FL3 channel of a Becton Dickinson FACScan.

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