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. Author manuscript; available in PMC: 2015 Jul 7.
Published in final edited form as: Cell Res. 2008 Jun;18(6):649–663. doi: 10.1038/cr.2008.57

Figure 1.

Figure 1

Induction of ESE-1 and ESE-3 mRNA expression, and ESE-1 protein expression by IL-1β and/or TNF-α in BEAS-2B human bronchial epithelial cells. (A, B) ESE-1 and ESE-3 mRNAs in BEAS-2B cells treated with IL-1β, TNF-α or a combination of IL-1β and TNF-α (Cyt), at 10 ng/ml each, for the indicated time periods (1–48 h). (C) ESE-1 protein in BEAS-2B cells treated with a combination of IL-1β and TNF-α, at 10 ng/ml each, for the indicated time periods. Nuclear extracts from treated and untreated cells were analyzed by western blotting with a polyclonal antibody specific for ESE-1. G3PDH was included as a protein loading control. (D, E). The effects of NF-κB inhibitors on cytokine-induced ESE-1 and ESE-3 mRNA expression. BEAS-2B cells were treated with increasing amounts of CAPE or Genistein (Gen.) as indicated for 2 h and then exposed to IL-1β and TNF-α (Cyt, at 10 ng/ml each) for 2 h (D) or 24 h (E). ESE-1 and ESE-3 mRNA expression was determined by real-time quantitative PCR. Values shown are the mean ± SD (n = 3), *P < 0.05 compared with the IL-1β+TNF-α group.

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