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. Author manuscript; available in PMC: 2014 Sep 15.
Published in final edited form as: Nature. 2012 Aug 30;488(7413):670–674. doi: 10.1038/nature11290

Fig. 1. Role of PKR in pyroptosis-mediated HMGB1 release.

Fig. 1

a-b. Cells were stimulated with Poly I:C. (a) Macrophages from PKR+/+ or PKR-/- mice. (b) PKR+/+ macrophages treated with indicated doses of the PKR inhibitor 2-AP. c. LPS-primed PKR+/+ macrophages were stimulated or treated with or without potassium-substituted medium (KCl) as indicated. Cells were lysed at indicated time points and PKR activation was monitored by autophosphorylation. d-g. LPS-primed PKR+/+ or PKR-/- macrophages were stimulated or treated with 2-AP as indicated. HMGB1 levels in the supernatant were determined by Western blot. Cytotoxicity was determined by LDH assay. Data shown are means ± SD of 3 independent experiments. #, p<0.05 vs. wild-type stimulated groups. h. Mass-spectrometric analysis of acetylation status of nuclear location sequences (NLS) of HMGB1.