Figure 2.
NLRP3 inflammasome activation is correlated to RAC2 activation level. HEK293T cells were transfected for 16 h with plasmids encoding the NLRP3 inflammasome components: myc-NLRP3, GFP-tagged ASC, mouse Caspase-1 (mCaspase1), and pro-IL-1β-Flag together with the WT form or the different mutants of RAC2 (HA-RAC2). Cleaved-IL-1β secretion in the culture supernatant (Sup) and protein expression in the cell lysates were assessed by immunoblotting. (A) RAC2 Q61R mutation was compared with WT and the constitutively active mutant RAC2 Q61E. (B) RAC2 D57N, D63V, and E62K mutations were compared with WT and the constitutively active mutant RAC2 Q61E. (C) G12R mutation was compared to WT and the constitutively active mutant RAC2 G12V. Data are representative for n = 3. Molecular weight (kD) is indicated in the figure. Source data are available for this figure: SourceData F2.

NLRP3 inflammasome activation is correlated to RAC2 activation level. HEK293T cells were transfected for 16 h with plasmids encoding the NLRP3 inflammasome components: myc-NLRP3, GFP-tagged ASC, mouse Caspase-1 (mCaspase1), and pro-IL-1β-Flag together with the WT form or the different mutants of RAC2 (HA-RAC2). Cleaved-IL-1β secretion in the culture supernatant (Sup) and protein expression in the cell lysates were assessed by immunoblotting. (A) RAC2 Q61R mutation was compared with WT and the constitutively active mutant RAC2 Q61E. (B) RAC2 D57N, D63V, and E62K mutations were compared with WT and the constitutively active mutant RAC2 Q61E. (C) G12R mutation was compared to WT and the constitutively active mutant RAC2 G12V. Data are representative for n = 3. Molecular weight (kD) is indicated in the figure. Source data are available for this figure: SourceData F2.

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