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Fig. 3 | Gut Pathogens

Fig. 3

From: CMTM3 protects the gastric epithelial cells from apoptosis and promotes IL-8 by stabilizing NEMO during Helicobacter pylori infection

Fig. 3

Proteomics analysis indicates that NEMO is involved in H. pylori-CMTM3-inflammation. a Differentially expressed proteins (P.adj < 0.05). b Kyoto Encyclopedia of Genes and Genomes. enrichment analysis. The TOP regulated signaling pathways were shown of CMTM3 KO vs control (LentiV2) in GES-1 cells (padj < 0.05). c Heat map of the expression levels of the differentially expressed proteins enriched in epithelial cell signaling in H. pylori infection signaling pathway. Red indicates high and blue indicates low protein expression. d NEMO expression was detected in CMTM3 KO GES-1 and HEK 293 T cells by western blotting. β-Actin was used as a control. Data are representative of three independent experiments. e NEMO expression was detected in CMTM3 KO GES-1 cells by qRT-PCR. Data is representative of three independent experiments. f Representative immunohistochemistry images of NEMO by human gastric tissues from the same patient before and after H. pylori infection (n = 11). g Summary of immunohistochemistry results for NEMO. Graph showing the average quantification of NEMO positive cells in at least 6 random fields of one patient. Data is expressed as means ± SEM. *p < 0.05. ns, no statistical difference

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