Fig. 4: Knockdown of NFE2L1 leads to reprogramming of glucose metabolism. | Cell Death & Disease

Fig. 4: Knockdown of NFE2L1 leads to reprogramming of glucose metabolism.

From: Dysfunction of the energy sensor NFE2L1 triggers uncontrollable AMPK signaling and glucose metabolism reprogramming

Fig. 4: Knockdown of NFE2L1 leads to reprogramming of glucose metabolism.

A The schematic diagram of glycolysis, gluconeogenesis, and TCA metabolism processes and key enzymes. B The expression of NFE2L1, HMOX1, PTGS1, and PTGS2 genes in HepG2shNC and HepG2shNFE2L1 cells as detected by qPCR; β-actin was used as the internal control. C The expression of HK1, HK2, PFKL, PFKM, PKM, PC, and DLD genes in HepG2shNC and HepG2shNFE2L1 cells as detected by qPCR; β-actin was used as the internal control. D The expression of CS, IDH1, IDH2, IDH3A, IDH3B, IDH3G, and OGDH genes in HepG2shNC and HepG2shNFE2L1 cells as detected by qPCR; β-actin was used as the internal control. E The expression of NFE2L1, G6PC3, FBP1, and PCK2 genes in HepG2shNC and HepG2shNFE2L1 cells as detected by qPCR; β-actin was used as the internal control. F The expression of NFE2L1, KEAP1, NFE2L2, HMOX1, PTGS2, HK1, PFKL, PKM, PC, IDH1, IDH2, PCK2, and β-actin in HepG2shNC and HepG2shNFE2L1 cells as detected by western blotting. G The expression of key enzymes for glucose metabolism in the transcriptome data. H The results of the metabolome showed the effect of NFE2L1 on central metabolism. n ≥ 3, *p < 0.05.

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