Fig. 5.
Fig. 5. Inhibitors of the NF-κB pathway reverse the protective effect of vFLIP K13 against growth factor withdrawal–induced apoptosis. / (A) TF-1 vector and vFLIP K13 cells were infected with adenoviral vectors expressing β-galactosidase (control) or a superrepressor form of IκBα(DN-IκBα) at a multiplicity of infection of 1000. Approximately 48 hours after infection, cells were grown in the absence or presence of GM-CSF for another 48 hours and cell viability measured using the MTS assay. The values shown are means ± SD of 2 independent experiments performed in triplicate. (B-E) TF-1 vector and vFLIP K13 cells were grown without GM-CSF and in the presence of indicated doses of drugs for 48 hours. Cell viability was measured using the MTS assay and percent cell survival calculated using the viability of cells grown in the presence of GM-CSF as 100%. The values shown are means ± SD of a representative of 2 independent experiments performed in triplicate.

Inhibitors of the NF-κB pathway reverse the protective effect of vFLIP K13 against growth factor withdrawal–induced apoptosis.

(A) TF-1 vector and vFLIP K13 cells were infected with adenoviral vectors expressing β-galactosidase (control) or a superrepressor form of IκBα(DN-IκBα) at a multiplicity of infection of 1000. Approximately 48 hours after infection, cells were grown in the absence or presence of GM-CSF for another 48 hours and cell viability measured using the MTS assay. The values shown are means ± SD of 2 independent experiments performed in triplicate. (B-E) TF-1 vector and vFLIP K13 cells were grown without GM-CSF and in the presence of indicated doses of drugs for 48 hours. Cell viability was measured using the MTS assay and percent cell survival calculated using the viability of cells grown in the presence of GM-CSF as 100%. The values shown are means ± SD of a representative of 2 independent experiments performed in triplicate.

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