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. Author manuscript; available in PMC: 2020 Mar 11.
Published in final edited form as: Nature. 2019 Sep 11;573(7775):590–594. doi: 10.1038/s41586-019-1551-2

Extended Data Fig. 5 |. Loss of DDX3X in BMDMs leads to the specific inhibition of NLRP3 inflammasome activation.

Extended Data Fig. 5 |

a–d, CASP1 cleavage in stimulated and unstimulated BMDMs and IL-1β and IL-18 release from BMDMs stimulated to activate the NLRP3, NLRC4, AIM2 and PYRIN inflammasomes by using LPS and nigericin (a) (ELISA, n > 10); flagellin (b) (ELISA, n = 2); poly(dA:dT) (c) (ELISA, n = 2); and Clostridium difficile toxin B (TcdB) (d) (ELISA, n = 2). P values in a (from left to right): *P = 0.0170, *P = 0.0116 (unpaired two-sided t-test); n.d., not detected. ELISA data are mean ± s.e.m. Representative blots (n = 3 biologically independent experiments each). e, Immunoblot analysis of CASP1 cleavage in wild-type BMDMs expressing a doxycycline-inducible DDX3X–mCherry construct and treated with LPS and nigericin. Representative blots (n = 2 biologically independent experiments). f, Immunoblot analysis of CASP1 cleavage in wild-type BMDMs and Ddx3xfl/flLysMcre BMDMs that constitutively express DDX3X–YFP from a cytomegalovirus promoter, treated with LPS and nigericin. Representative blots (n = 2 biologically independent experiments).