ArticleProceedings of the National Academy of Sciences of the United States of America1998
Ectopic expression of N-acetylglucosaminyltransferase III in transgenic hepatocytes disrupts apolipoprotein B secretion and induces aberrant cellular morphology with lipid storage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Identification of biomarkers between coronary artery disease and non-alcoholic steatohepatitis: a combination of bioinformatics and machine learning.Frontiers in genetics · 2025Article
- VLDL Biogenesis and Secretion: It Takes a Village.Circulation research · 2024Review
- Review
- Genomic and transcriptomic somatic alterations of hepatocellular carcinoma in non-cirrhotic livers.Cancer genetics · 2022Article
- GLT25D2 Is Critical for Inflammatory Immune Response to Promote Acetaminophen-Induced Hepatotoxicity by Autophagy Pathway.Frontiers in pharmacology · 2020Article
- Article
- The glycomic effect of N-acetylglucosaminyltransferase III overexpression in metastatic melanoma cells. GnT-III modifies highly branched N-glycans.Glycoconjugate journal · 2018Article
- Improving Immunotherapy Through Glycodesign.Frontiers in immunology · 2018Review
- DNA hypomethylation upregulates expression of the MGAT3 gene in HepG2 cells and leads to changes in N-glycosylation of secreted glycoproteins.Scientific reports · 2016Article
- Glycosyltransferases and non-alcoholic fatty liver disease.World journal of gastroenterology · 2016Review
- Mechanism of the effect of glycosyltransferase GLT8D2 on fatty liver.Lipids in health and disease · 2015Article
- Glycosyltransferase GLT8D2 positively regulates ApoB100 protein expression in hepatocytes.International journal of molecular sciences · 2013Article
- Cloning and expression analysis of cDNAs corresponding to genes activated in cucumber showing systemic acquired resistance after BTH treatment.BMC plant biology · 2004Article
- Antibodies that recognize bisected complex N-glycans on cell surface glycoproteins can be made in mice lacking N-acetylglucosaminyltransferase III.Glycoconjugate journal · 2002Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Acetylglucosaminyltransferase III (GnT-III) produces "bisecting-GlcNAc" and regulates the branching of N-glycans. GnT-III activity is elevated during hepatocarcinogenesis, which is in contrast to the undetectable level found in normal hepatocytes. To determine the biological significance of GnT-III in hepatocytes, transgenic mice that specifically express GnT-III in the liver were established and characterized. The transgenic hepatocytes had a swollen oval-like morphology, with many lipid droplets. Apolipoprotein B, which contained increased level of bisecting-GlcNAc accumulated in the transgenic hepatocytes. In the transgenic serum, triglycerides, the beta- and pre-beta-lipoprotein fractions, and apolipoprotein B100 were significantly decreased, compared with levels in nontransgenic serum. These abnormal phenotypes were more prominent in the mice with more copies of the transgene and a resulting high GnT-III activity. We demonstrate that aberrant glycosylation, as the direct result of the formation of bisecting-GlcNAc, disrupts the function of apolipoprotein B, leading to the generation of fatty liver. This observation suggests a novel mechanism for the pathogenesis of fatty liver.
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