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. Author manuscript; available in PMC: 2012 Oct 16.
Published in final edited form as: Mol Carcinog. 2010 Sep;49(9):837–848. doi: 10.1002/mc.20660

Figure 2.

Figure 2

JNK and PI3K signaling cascades contribute to LPS-induced Pdcd4 regulation. (A) RAW264.7 macrophages were stimulated with LPS (100 ng/mL) for 0–12 h, then subjected to Western blotting for the detection of phosphorylation of MAPKs (ERK1/2, JNK1/2, and p38), c-jun, and PI3K using appropriate antibodies. The expression levels of the nonphosphorylated forms did not differ significantly among the treatments (data not shown). Results shown are representative of three independent experiments. (B) RAW264.7 macrophages were preincubated with vehicle (0.5% DMSO), PD98059 (MEK inhibitor), SP600125 (JNK inhibitor), SB203580 (p38 inhibitor), or LY294002 (PI3K inhibitor) for 30 min, then treated with or without LPS (100 ng/mL). After 24 h of incubation, total RNA was isolated for RT-PCR. Each value represents the mean ± SD of at least three independent experiments. Student’s t-test was used to determine significant differences. aP <0.005 versus control, bP <0.05 versus LPS.