Fig. 5.
Fig. 5. Caspase-8 activation is critical for potentiation of paclitaxel lethality by bryostatin 1. / U937 cells ectopically expressing dominant-negative caspase-8 (U937/casp8-DN) and CrmA were treated with paclitaxel (5 nM) with or without bryostatin 1 (10 nM) or treated with TNF-α (1 ng/mL) plus CHX (1 μM) for 24 hours. Apoptotic cells were quantified by annexin V and PI positivity as described in “Materials and methods.” Results shown are representative of 3 experiments (means ± SE) employing several U937/casp8-DN and U937/CrmA clones. *Significant difference relative to empty-vector control cells (P < .01).

Caspase-8 activation is critical for potentiation of paclitaxel lethality by bryostatin 1.

U937 cells ectopically expressing dominant-negative caspase-8 (U937/casp8-DN) and CrmA were treated with paclitaxel (5 nM) with or without bryostatin 1 (10 nM) or treated with TNF-α (1 ng/mL) plus CHX (1 μM) for 24 hours. Apoptotic cells were quantified by annexin V and PI positivity as described in “Materials and methods.” Results shown are representative of 3 experiments (means ± SE) employing several U937/casp8-DN and U937/CrmA clones. *Significant difference relative to empty-vector control cells (P < .01).

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