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. 2021 Nov 2;297(6):101379. doi: 10.1016/j.jbc.2021.101379

Figure 2.

Figure 2

CASP6 is not involved in priming the CASP11-NLRP3 inflammasome during gram-negative bacterial infections. A, immunoblot analysis of phosphorylated ERK (pERK), phosphorylated IκB (pIκB), total ERK (tERK), and total IκB (tIκB) in bone marrow-derived macrophages (BMDMs) after Escherichia coli (20 MOI) infection for the indicated time. Actin was used as the internal control. B, immunoblot analysis of pERK, pIκB, tERK, and tIκB in BMDMs after Citrobacter rodentium (20 MOI) infection for the indicated time. Actin was used as the internal control. C, immunoblot analysis of NLRP3, CASP11, pro–IL-1β, and ASC in BMDMs after E. coli (20 MOI) infection for the indicated time. Actin was used as the internal control. D, immunoblot analysis of NLRP3, CASP11, pro–IL-1β, and ASC in BMDMs after C. rodentium (20 MOI) infection for the indicated time. Actin was used as the internal control. The data are representative of at least three independent experiments. ASC, apoptosis-associated speck-like protein containing a CARD; CASP, caspase; ERK, extracellular signal-regulated kinase; MOI, multiplicity of infection; NLRP, nucleotide-binding oligomerization domain-like receptor containing pyrin domain.