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Published byΛίγεια Δοξαράς Modified over 5 years ago
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Figure 2. p62−/−MEF cells enhance the activation of NF-κB induced by TLR4. (A) Wild-type (WT) p62+/+MEF and p62−/−MEF cells were transfected with pBIIx-luc and Renilla luciferase vector, untreated or treated with LPS (1 µg/ml) for 6 h, then subjected to the luciferase activity assay. Results are expressed as fold-induction in luciferase activity relative to untreated cells. All error bars represent the mean±SD of triplicate samples. (B and C) WT p62+/+MEF and p62−/−MEF cells were untreated or treated with LPS (1 µg/ml) for 6 h, then analyzed for p65-DNA (B) or p50-DNA (C) binding activity. All error bars represent the mean±SD of triplicate samples. (D-F) WT p62+/+MEF and p62−/−MEF cells were untreated or treated with LPS (1 µg/ml) for 9 h, then subjected to ELISA to determine the levels TNF-α (D), IL-6 (E), and IL-1β (F) produced. All error bars represent the mean±SD from triplicate samples.WO, untreated; W LPS, treated with LPS. Figure 2. p62−/−MEF cells enhance the activation of NF-κB induced by TLR4. (A) Wild-type (WT) p62+/+MEF and p62−/−MEF cells were transfected with pBIIx-luc and Renilla luciferase vector, untreated or treated with LPS (1 µg/ml) for 6 h, then subjected to the luciferase activity assay… Immune Netw Jun;19(3):e16.
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