Fig. 4.
Fig. 4. Specific inhibition of NF-κB with Bay 11-7082. / (A), The PEL cells BC1, BC2, BC3, and control BJAB cells were treated with Bay 11 and assessed for NF-κB and Oct-1/DNA binding. Cells were placed in culture at 7.5 × 105 cells/mL and treated with 5 μmol/L Bay 11. After 1 hour and 24 hours, nuclear proteins were extracted and EMSAs performed using NF-κB– or Oct-1–specific radiolabeled oligonucleotide probes. All PEL cell lines demonstrated inhibition of NF-κB/DNA binding within 1 hour of treatment but demonstrated no inhibition of Oct-1/DNA binding. The specificity of the NF-κB inhibition was maintained throughout the 24-hour assay in each cell line. (B), The PEL cells BC1, BC2, and BC3 were treated with 5 μmol/L Bay 11 for 24 hours and assessed by immunoblot for total and phosphorylated p38. All cell lines showed the presence of phosphorylated p38, but the levels of p38 activation were not affected by treatment with Bay 11.

Specific inhibition of NF-κB with Bay 11-7082.

(A), The PEL cells BC1, BC2, BC3, and control BJAB cells were treated with Bay 11 and assessed for NF-κB and Oct-1/DNA binding. Cells were placed in culture at 7.5 × 105 cells/mL and treated with 5 μmol/L Bay 11. After 1 hour and 24 hours, nuclear proteins were extracted and EMSAs performed using NF-κB– or Oct-1–specific radiolabeled oligonucleotide probes. All PEL cell lines demonstrated inhibition of NF-κB/DNA binding within 1 hour of treatment but demonstrated no inhibition of Oct-1/DNA binding. The specificity of the NF-κB inhibition was maintained throughout the 24-hour assay in each cell line. (B), The PEL cells BC1, BC2, and BC3 were treated with 5 μmol/L Bay 11 for 24 hours and assessed by immunoblot for total and phosphorylated p38. All cell lines showed the presence of phosphorylated p38, but the levels of p38 activation were not affected by treatment with Bay 11.

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