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. 2008 Jun 23;112(6):2474–2483. doi: 10.1182/blood-2007-12-130211

Figure 4.

Figure 4

TAT-NPMΔC inhibits NF-κB activation. (A) Effect of TAT-NPMΔC on TNF-α–induced nuclear translocation of NF-κB. HEK293T cells were first treated with BSA, TAT-NPM, or TAT-NPMΔC (30 μg/mL each) for 30 minutes then stimulated with TNF-α (10 ng/mL) for 30 minutes. Nuclear localization of the NF-κB subunit p65 in the nuclear extracts was analyzed by immunoblot analysis of the NF-κB subunit p65. (B) Effect of TAT-NPMΔC on TNF-α–induced DNA-binding activity of NF-kB. HEK293T cells were first treated with BSA, TAT-NPM, or TAT-NPMΔC (30 μg/mL each) for 30 minutes then stimulated with TNF-α (10 ng/mL) for the indicated time. Nuclear extracts were then prepared and DNA-binding activity of NF-κB was measured by transcription factor enzyme-linked immunosorbent assay (ELISA). Data are presented as fold activation relative to the DNA-binding activity in BSA-treated cells without TNF-α stimulation. (C) TAT-NPMΔC prolongs TNF-α–induced nuclear accumulation of NF-κB. HEK293T cells were first treated with BSA, TAT-NPM, or TAT-NPMΔC (30 μg/mL each) for 30 minutes then stimulated with TNF-α (10 ng/mL) for the indicated time. Nuclear localization of the NF-κB subunit p65 in the nuclear extracts was analyzed by immunoblot analysis of the NF-κB subunit p65. (D) TAT-NPMΔC inhibits NF-κB transcriptional activity. HEK293T cells transfected with a 3 × κB-Luc plasmid were treated with BSA, TAT-NPM, or TAT-NPMΔC (30 μg/mL each) for 30 minutes, then stimulated with TNF-α (10 ng/mL) for another 30 minutes. Results of triplicate experiments are shown with mean and standard deviation.