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. 2006 Feb 13;103(8):2953–2958. doi: 10.1073/pnas.0510802103

Fig. 2.

Fig. 2.

IL-1β-mediated activation of Src, but not Akt, depends on the recruitment of MyD88. Representative Western blots are shown, and bar graphs indicate means ± SEM from at least three independent experiments. (A and B) Cultured wild-type AH neurons were developed on a preformed bed of glia from IL-1RI−/− mice. Neurons were stimulated with IL-1β (10–12 nM) for 10 min after a 15-min exposure to the TIR domain mimetics AS-1 (20 μM), EM77 (20 μM), or EM110 (20 μM). The IL-1β stimulations in the presence of drug in A were not statistically significant compared with IL-β treatment (P > 0.05). (C and D) Cultured AH neurons from MyD88−/− mice were developed on a preformed bed of glia from IL-1RI−/− mice. Neurons were stimulated with IL-1β (10–12 nM) for 10 min after a 15-min exposure to the MyD88 mimetic AS-1 (100 μM) and the PI3-kinase inhibitor LY294002 (20 μM) (C) or the Src-family inhibitor PP2 (2 μM) (D). Statistical significance was determined by ANOVA followed by Tukey’s test; significance is indicated with an ∗ compared with control and a ∗∗ compared with IL-1β treatment at P < 0.05.