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. Author manuscript; available in PMC: 2022 Aug 25.
Published in final edited form as: Nature. 2018 Nov 28;564(7734):71–76. doi: 10.1038/s41586-018-0761-3

Figure 6. Binding to PI4P on dTGN is essential for K+ efflux-independent NLRP3 activation.

Figure 6.

a, HeLa cells stably expressing the indicated proteins were treated −/+ imiquimod or CL097 (45 μg/mL) for 80 minutes before cell lysates were analyzed by the in vitro NLRP3 activity assay. b, c, Primary ASC-deficient BMDMs were primed with LPS and incubated −/+ imiquimod or CL097 (45 μg/mL) for 60 minutes. The percentage of cells with NLRP3 puncta on dTGN was quantified from 100 cells (n = 3, mean ± SD, two-sided t test). N.D., not detectable. d, Primary NLRP3-deficient BMDMs reconstituted with the indicated proteins were primed with LPS and treated −/+ imiquimod. Cell lysates (lys) and supernatants (sup) were analyzed by immunoblotting with the indicated antibodies to assess the inflammasome activation. e, HeLa cells stably expressing the indicated NLRP3 proteins were treated −/+ imiquimod in the presence of increasing concentrations of KCl and the cell lysates were analyzed by the in vitro NLRP3 activation assay.