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. 2021 Apr 28;7(18):eabd4742. doi: 10.1126/sciadv.abd4742

Fig. 4. METTL3 deficiency impairs the TLR4 signaling pathway by modulating IRAKM expression.

Fig. 4

(A) Activation of the TLR4 signaling pathway in Mettl3-KO and Mettl3-WT BMDMs upon LPS stimulation was analyzed by Western blotting of p65, JNK, p38, ERK, and IRAKM. (B) Relative expression of Tirap, Myd88, Traf6, Irak, Irak4, Trif, and Tram in Mettl3flox/flox;Lyzm-Cre mice and Mettl3flox/flox littermates measured by real-time qPCR. (C) Relative expression of Irakm in control (NT) and LPS-treated Mettl3flox/flox;Lyzm-Cre and Mettl3flox/flox littermates measured by real-time qPCR. (D) Knockdown efficiency of shRNA targeting Irakm in BMDMs measured by real-time qPCR (n = 3). (E) TNF-α synthesis in WT BMDMs transfected with control shRNA (sh-CTL) and Mettl3-deficient BMDMs transfected with sh-CTL or IRAKM shRNA (sh-IRAKM) measured by flow cytometry (n = 3). Data are shown as representative results of three independent experiments (A) or as means ± SEM (B to E). **P < 0.01 and ***P < 0.001 (unpaired two-tailed Student’s t test).