Contribution of BK channels to TNF-α release and signaling from LPS-stimulated BMDM. (A) BK^+/+ BMDMs were stimulated with indicated concentrations of LPS resulting in a dose-dependent TNF-α release. TNF-α release was inhibited by paxilline and IbTX in a dose-dependent fashion. Bars (mean ± SD from 3 experiments). (B,C) LPS stimulation (10 ng/mL) triggered similar TNF-α release in BK^+/+ and BK^−/− BMDMs as shown by individual results (B) and mean plus or minus SD (C) from 9 experiments. (D) IκB-α degradation, Akt phosphorylation, and ERK phosphorylation were similar in BK^+/+ and BK^−/− BMDMs, as assayed by immunoblots.