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Literature summary for 2.4.1.155 extracted from

  • Cui, J.; Huang, W.; Wu, B.; Jin, J.; Jing, L.; Shi, W.P.; Liu, Z.Y.; Yuan, L.; Luo, D.; Li, L.; Chen, Z.N.; Jiang, J.L.
    N-glycosylation by N-acetylglucosaminyltransferase V enhances the interaction of CD147/basigin with integrin beta1 and promotes HCC metastasis (2018), J. Pathol., 245, 41-52 .
    View publication on PubMedView publication on EuropePMC
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Cloned(Commentary)

Cloned (Comment) Organism
gene MGAT5, quantitative real-time PCR enzyme expression analysis Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information GnT-V enzyme silencing by siRNA in Huh-7 and HepG2 cells Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q09328
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Source Tissue

Source Tissue Comment Organism Textmining
Hep-G2 cell
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 Homo sapiens
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hepatoma cell
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 Homo sapiens
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Huh-7 cell
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 Homo sapiens
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liver
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
GnT-V
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 Homo sapiens
mannoside acetylglucosaminyltransferase 5
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 Homo sapiens
Mgat5
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 Homo sapiens
N-acetylglucosaminyltransferase V
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 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens the PI3K/Akt signaling pathway is involved in regulation of GnT-V expression additional information

General Information

General Information Comment Organism
malfunction interruption of beta1,6-GlcNAc glycan modification of CD147/basigin decreases matrix metalloproteinase (MMP) expression in HCC cell lines and affects the interaction of CD147/basigin with integrin beta1, mechanism modeling, overview. Real-time PCR shows that MMP-1, MMP-2, and MMP-9 are reduced in cells treated with mutant CD147/basigin (defective beta1,6-branched N-glycosylation) compared with cells treated with wild-type, suggesting that GnT-V-mediated glycosylation increases CD147/basigin-mediated HCC cell invasion. Overexpression of GnT-V increases the level of CD147/basigin-beta1,6-branching and the induction of MMPs Homo sapiens
metabolism activation of the PI3K/Akt pathway is involved in the regulation of GnT-V expression and deletion of GnT-V-mediated N-glycosylation impairs the PI3K/Akt pathway Homo sapiens
physiological function alterations in glycosylation patterns regulate cancer development and progression, serve as important biomarkers, and provide a set of specific targets for diagnosis and therapeutic intervention. The modifications most often associated with cancer include sialylation, beta1,6-GlcNAc-branched N-glycans, and core fucosylation. Increased GlcNAc-branched N-glycan levels result from increased activity of N-acetylglucosaminyltransferase V (GnT-V) encoded by the mannoside acetylglucosaminyltransferase 5 (MGAT5) gene and are closely associated with cancer metastasis. N-acetylglucosaminyltransferase V (GnT-V) regulates cancer processes and cancer cell migration. GnT-V-mediated N-glycosylation of CD147/basigin, a tumor-associated glycoprotein that carries beta1,6-N-acetylglucosamine (beta1,6-GlcNAc) glycans, is upregulated during TGF-beta1-induced epithelial-to-mesenchymal transition (EMT), which correlates with tumor metastasis in patients with hepatocellular carcinoma (HCC). The PI3K/Akt signaling pathway is involved in the regulation of GnT-V expression Homo sapiens