Skip to main content
. Author manuscript; available in PMC: 2020 Apr 25.
Published in final edited form as: Cell Rep. 2020 Jan 21;30(3):699–713.e4. doi: 10.1016/j.celrep.2019.12.073

Figure 4. IFN Signaling Antagonizes RIPK in the Activation of eIF4E- and mTORC1-Mediated Translation.

Figure 4.

(A) TNF-α and CXCL-1 protein levels after indicated stimulations ± treatment with eIF4E inhibitor 4EGi-1 in B6, Ifnb−/−, and RIP1 Ki Ifnb−/− BMDMs.

(B) p-eIF4E and total 4E-BP levels in B6, Ifnb−/−, and RIP1 Ki BMDMs stimulated as indicated ± 5 IU IFNβ priming overnight.

(C) TNF-α and CXCL-1 protein levels after indicated stimulations ± treatment with mTORC1 inhibitor Torin 2 in B6, Ifnb−/−, and RIP1 Ki Ifnb−/− BMDMs.

(D and E) Cell death as measured by propidium iodide incorporation over 6 h in B6, Ifnb−/−, and RIP1 Ki Ifnb−/− BMDMs stimulated with LZ ± treatment with 4EGi-1 (D) or Torin 2 (E).

(F) TNF-α and CXCL-1 protein levels after indicated stimulations ± overnight treatment with IFNAR-blocking antibody (αIFNAR) in Akt1−/− and wild-type (WT) littermate BMDMs.

In all panels, BMDMs were stimulated with LPS, LZ, LZNs, Z, Ns, or LZN as indicated. ELISA and qPCR data are shown as ±SD from three independent experiments compared using two-way ANOVA: n.s. (p > 0.05), *p < 0.05, and ****p < 0.0001. Western blot and kinetic cell death experiments are representative of three or more independent experiments. Kinetic data are presented as the mean ± SD of triplicate wells.

See also Figures S4 and S5.