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. 2022 Aug 5;189(2):186–202. doi: 10.1093/toxsci/kfac080

Figure 5.

Figure 5.

Nicotine-induced downregulation of SLBP is regulated by CK2. A and B, Inhibition of CK2 attenuates nicotine-induced downregulation of SLBP. BEAS-2B cells were treated with or without nicotine for 24 h in the presence or absence of DMAT, an CK2 inhibitor, and subjected to Western blot (A). The band intensities were quantified and presented as bar graphs to show relative quantifications of SLBP (B). GAPDH was used as an internal control. C–F, Knockdown of CK2α1 by siRNA attenuates nicotine-induced downregulation of SLBP and phosphorylation of AKT at S473. BEAS-2B cells were transiently transfected with control siRNA or CK2α1 siRNA and then treated with or without nicotine for 24 h followed by Western blot analysis with indicated antibodies (C). The band intensities were quantified and presented as bar graphs to show relative quantifications of CK2α1 (D), p-AKTS473/AKT (E), and SLBP (F). GAPDH was used as an internal control. G–J, Knockdown of CK2α2 by siRNA has no effects on nicotine-induced downregulation of SLBP. BEAS-2B cells were transiently transfected with control siRNA or CK2α2 siRNA and then treated with or without nicotine for 24 h followed by Western blot analysis with indicated antibodies (G). The band intensities were quantified and presented as bar graphs to show relative quantifications of CK2α2 (H), p-AKTS473/AKT (I), and SLBP (J). GAPDH was used as an internal control. Untreated controls in lane 1 were used as references, which were set to 1. The data shown are the mean ± SD (n = 3). *p < .05 versus untreated control group; &p < .05 versus control group in Ctrl siRNA cells in panel K.