Fig. 1: Expression of cytokines is highly induced during necroptosis.
From: Necroptosis promotes cell-autonomous activation of proinflammatory cytokine gene expression
a The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database analysis of the 813 necroptosis-upregulated genes in Enrichr. b Scatterplot of the fold inductions of the overlapping genes induced by TNFα and TSZ. Representative genes were labeled. c Table of selected proteins identified in the media of necroptotic cells by mass spectrometry. Protein abundance was quantified with LFQ module implemented in MaxQuant. d HT-29 cells were treated with TSZ for the indicated periods of time. Cxcl8, Cxcl1, and Cxcl2 mRNA levels were measured by qPCR. The cell viability was determined by CellTiter-Glo. e HT-29 cells were treated with TSZ for the indicated periods of time. The cell lysates and culture media were collected separately, and analyzed by western blotting with indicated antibodies. f HT-29 cells were treated as indicated for 8 h. The expression levels of Cxcl8 and Cxcl1 were analyzed by qPCR. The cell viability was determined by CellTiter-Glo. D, DMSO (<0.2%). g HT-29 cells were treated as indicated for 8 h. The supernatants and cell lysates were collected and analyzed by western blotting. h MEFs were treated for the indicated periods of time with TSZ. The expression levels of Cxcl2 and Csf2 were determined by qPCR. The cell viability was determined by CellTiter-Glo. i MEFs were treated as indicated. Cxcl2 and Csf2 mRNA levels were measured by qPCR after 4 h of treatment. The cell viability was determined by CellTiter-Glo after 13 h of treatment. Gene expression determined by qPCR was shown as fold induction compared with untreated cells in all figures. All reagents were used at concentrations as described in Materials and Methods in all experiments, unless otherwise noted. Data were presented as mean ± SEM of triplicates
