Abstract:Enhanced green fluorescent protein (EGFP) is a widely used biological reporter. However, the effects of EGFP expression in vivo are still unclear. To investigate the effects of EGFP transgenic expression in vivo, we employed an NMR-based metabonomics method to analyze the metabonome of EGFP transgenic mice. The results show that the metabonomes of urine, liver, and kidney of the EGFP transgenic mice are different from their wild-type counterparts. The EGFP mice expressed high levels of urinary 3-ureidopropiona… Show more
“…3 ) in which FABP1 binds a specifi c ligand, the complex stimulates a transcription factor, which then upregulates FABP1 expression. FABP1 overexpression may reduce ligand been found to have some biological effects ( 121,122 ) and could specifi cally affect in vivo nucleic acid metabolism, energy utilization, amino acid catabolism, and immune responses ( 123,124 ). Also, composition of diets, gender, and age of animals all vary between studies.…”
“…3 ) in which FABP1 binds a specifi c ligand, the complex stimulates a transcription factor, which then upregulates FABP1 expression. FABP1 overexpression may reduce ligand been found to have some biological effects ( 121,122 ) and could specifi cally affect in vivo nucleic acid metabolism, energy utilization, amino acid catabolism, and immune responses ( 123,124 ). Also, composition of diets, gender, and age of animals all vary between studies.…”
“…Additionally, metabolomics analysis tools such as nuclear magnetic resonance spectroscopy (NMR) are commonly utilized in the evaluation of the systematic responses to exogenous stimuli2122. In the case of HBV infection, approaches such as metabolomics, proteomics, and molecular biology assays have been utilized to identify the central carbon metabolism, hexosamine pathway, and disruption of nucleotide synthesis in HepG2.2.15 cells23.…”
Chronic hepatitis B virus (HBV) infection is partly responsible for hepatitis, fatty liver disease and hepatocellular carcinoma (HCC). HBV core protein (HBc), encoded by the HBV genome, may play a significant role in HBV life cycle. However, the function of HBc in the occurrence and development of liver disease is still unclear. To investigate the underlying mechanisms, HBc-transfected HCC cells were characterized by multi-omics analyses. Combining proteomics and metabolomics analyses, our results showed that HBc promoted the expression of metabolic enzymes and the secretion of metabolites in HCC cells. In addition, glycolysis and amino acid metabolism were significantly up-regulated by HBc. Moreover, Max-like protein X (MLX) might be recruited and enriched by HBc in the nucleus to regulate glycolysis pathways. This study provides further insights into the function of HBc in the molecular pathogenesis of HBV-induced diseases and indicates that metabolic reprogramming appears to be a hallmark of HBc transfection.
“…Metabolomics analysis method combining multivariate data analysis and spectral profile techniques, such as magnetic resonance spectroscopy (NMR), provides metabolic information and has been successfully applied in the evaluation of the systematic responses to exogenous stimuli 8 9 . Importantly, the results from metabolomics studies provide comprehensive information, enabling the generation of credible hypotheses, which can then be further validated by molecular biological assays.…”
Chronic infection caused by the hepatitis B virus (HBV), is strongly associated with hepatitis, fatty liver and hepatocellular carcinoma. To investigate the underlying mechanisms, we characterize the metabolic features of host cells infected with the virus using systems biological approach. The results show that HBV replication induces systematic metabolic alterations in host cells. HBV infection up-regulates the biosynthesis of hexosamine and phosphatidylcholine by activating glutamine-fructose-6-phosphate amidotransferase 1 (GFAT1) and choline kinase alpha (CHKA) respectively, which were reported for the first time for HBV infection. Importantly suppressing hexosamine biosynthesis and phosphatidylcholine biosynthesis can inhibit HBV replication and expression. In addition, HBV induces oxidative stress and stimulates central carbon metabolism and nucleotide synthesis. Our results also indicate that HBV associated hepatocellular carcinoma could be attributed to GFAT1 activated hexosamine biosynthesis and CHKA activated phosphatidylcholine biosynthesis. This study provides further insights into the pathogenesis of HBV-induced diseases, and sheds new light on drug target for treating HBV infection.
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