Skip to main content
. 2015 Apr 10;1(3):e1400139. doi: 10.1126/sciadv.1400139

Fig. 3. The downstream cytokines activated by CU-T12-9.

Fig. 3

(A) TLR1/2 signaling pathway after NF-κB activation. Ligands from Gram-positive bacteria, yeast, or fungi can induce the TLR1/2 dimerization, leading to the NF-κB activation through the adaptor proteins MyD88/TRAF/IKK. This triggers the SEAP promoter to secrete alkaline phosphatase or induces production of proinflammatory cytokines, such as TNF-α, IL, IFN, and NO (23, 29). (B and C) Dose-dependent activation of NO production in Raw 264.7 macrophage cells (B) and primary macrophage cells (C). Data are means ± SD. *P < 0.05 for CU-T12-9 relative to positive control. (D) ELISA assay results showed that CU-T12-9 activates the TNF-α production in Raw 264.7 macrophage cells with an EC50 of 60.46 ± 16.99 nM. Pam3CSK4 was used as a positive control in the experiment. Data are means ± SD. **P < 0.01 for CU-T12-9 (1.2 μM) relative to positive control.