Fig. 3.
Fig. 3. Inhibition of NF-κB activation by As2O3 in HTLV-1–infected cells. / (A) Sixty micrograms cytoplasmic protein was resolved on 10% to 20% Tris-glycine, transferred to PVDF membranes, and probed with an antibody specific for the phosphorylated form of IκBα. Results are representative of 2 independent experiments. (B) Comparable protein loading was verified using an antibody specific for the housekeeping gene product β-tubulin. Results are representative of 2 independent experiments. (C) Electrophoretic mobility shift assay using a previously published NF-κB–specific probe43 mixed with no extract (lane 1), mixed with 5 μg nuclear extract obtained from MT-2 treated with control buffer (lane 2), or treated with As2O3 + IFN-α and run on a 6% DNA retardation gel (lane 3). Specificity of the NF-κB binding was checked by competition with a 50-fold excess of cold probe (data not shown).

Inhibition of NF-κB activation by As2O3 in HTLV-1–infected cells.

(A) Sixty micrograms cytoplasmic protein was resolved on 10% to 20% Tris-glycine, transferred to PVDF membranes, and probed with an antibody specific for the phosphorylated form of IκBα. Results are representative of 2 independent experiments. (B) Comparable protein loading was verified using an antibody specific for the housekeeping gene product β-tubulin. Results are representative of 2 independent experiments. (C) Electrophoretic mobility shift assay using a previously published NF-κB–specific probe43 mixed with no extract (lane 1), mixed with 5 μg nuclear extract obtained from MT-2 treated with control buffer (lane 2), or treated with As2O3 + IFN-α and run on a 6% DNA retardation gel (lane 3). Specificity of the NF-κB binding was checked by competition with a 50-fold excess of cold probe (data not shown).

Close Modal

or Create an Account

Close Modal
Close Modal