Figure 2.
Figure 2. Characterization of the IκBα32/36A inducibility after doxycycline treatment. (A) Western blot detection of IκBα protein in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. (B) NF-κB binding activity assessed by EMSA in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. (C) Schematic representation of the transcriptional regulatory element of the IκBα promoter with its 3 κB sites in front of the luciferase gene (construct 0.4SK-luc). (D) Relative NF-κB transcriptional activity in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. Presented results correspond to the mean of 3 transfection experiments with the 0.4SK-luc construct. Each transfection experiment was conducted in triplicate.

Characterization of the IκBα32/36A inducibility after doxycycline treatment. (A) Western blot detection of IκBα protein in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. (B) NF-κB binding activity assessed by EMSA in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. (C) Schematic representation of the transcriptional regulatory element of the IκBα promoter with its 3 κB sites in front of the luciferase gene (construct 0.4SK-luc). (D) Relative NF-κB transcriptional activity in MS4A-IκBα32/36A-transfected cells with (+) or without (−) doxycycline at 2 μg/mL. Presented results correspond to the mean of 3 transfection experiments with the 0.4SK-luc construct. Each transfection experiment was conducted in triplicate.

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