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. 2022 Jun 14;13:3426. doi: 10.1038/s41467-022-31132-7

Fig. 3. Synergistic activation of TBK1 by CXCL4 and TLR8 drives inflammatory gene expression.

Fig. 3

a Immunoblots of phospho-TBK1 and total TBK1 with whole-cell lysates under the indicated conditions. β-actin serves as a loading control. b Representative flow cytometry plot (left) and bar graph showing cumulative data (right) of IRF3 phosphorylation after CXCL4 and ORN8L costimulation for 1 h and 3 h (n = 5 independent experiments). c qPCR analysis of IFNB1 mRNA normalized relative to GAPDH mRNA (n = 2). d–g qPCR analysis of the indicated mRNAs normalized relative to GAPDH mRNA. TBK1/IKKε were inhibited using MRT67307 (10 μM) (d, e), or GSK8612 (50 μM) or TBK1/IKKε-IN-2 (1 μM) (f) (n = 4 healthy donors), or knocked down using siRNA (g). h Immunoblot with whole-cell lysates under the indicated conditions. Data are representative of 3 (a, h), or show cumulative data for 4 (d–f), or 6 (g) independent experiments and depicted as mean ± SEM. ****p ≤ 0.0001; **p ≤ 0.01; *p ≤ 0.05 by Friedman test (b, g) or two-way ANOVA (d, e, f). Source data are provided as a Source data file.