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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: O-GlcNAc of STING mediates antiviral innate immunity

Fig. 1

HSV-1 Infection Activates Glucose Metabolism. A and B C57BL/6 mice (6 weeks old) were challenged with HSV-1 (5 × 10.6 PFU/mouse) for 6 days. The spleens of mice were collected for a targeted metabolomics assay. Glucose metabolites determined by LC–MS/MS metabolomics were assessed by principle-component analysis (A) and pathway-enrichment analysis (B). C Metabolites in the glycolysis, PPP, and HBP. D–G Heatmap of glucose metabolites (D) and fold changes of intermediate metabolites in the glycolysis (E), PPP (F), and HBP (G) in HSV-1-treated mice. H Levels of UDP-GlcNAc in the serum of non-treated and HSV-1-challenged mice were determined with an UDP-GlcNAc kit. I O-GlcNAc in KYSE-30 cells transfected with poly(dA:dT) (2 μg/mL) or treated with HSV-1 (MOI = 1) was detected with immunoblotting. Quantification of immunoblots was performed with ImageJ. Data are representatives of 3 independent biological replicates. Data are means ± SEM. * p < 0.05, *** p < 0.0001

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