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Literature summary for 2.4.1.144 extracted from

  • Lu, J.; Isaji, T.; Im, S.; Fukuda, T.; Kameyama, A.; Gu, J.
    Expression of N-acetylglucosaminyltransferase III suppresses alpha2,3-sialylation, and its distinctive functions in cell migration are attributed to alpha2,6-sialylation levels (2016), J. Biol. Chem., 291, 5708-5720.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
enzyme overexpression in HeLa-S3, CHO-K1, Pro-5, and MDA-MB-231 cells using vector CSIV-TRE-RfA-CMV-KT, cloning in HEK-293T cells Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information overexpression of GnT-III significantly inhibits alpha2,3-sialylation but not alpha2,6-sialylation. The migratory ability of cells, HeLa-S3, CHO-K1 and Pro-5, without or with a low level of alpha2,6-sialylation is consistently suppressed after overexpression of GnT-III, while in alpha2,6-hypersialylated MDA-MB-231 and MKN-45 cells little effects are observed. Phenotypes, detailed overview Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q09327
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Source Tissue

Source Tissue Comment Organism Textmining
glioma cell
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Homo sapiens
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HEK-293T cell
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Homo sapiens
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HeLa-S3 cell
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Homo sapiens
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hepatoma cell
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Homo sapiens
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MDA-MB-231 cell
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Homo sapiens
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ovarian cancer cell
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Homo sapiens
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Synonyms

Synonyms Comment Organism
GnT-III
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Homo sapiens
N-acetylglucosaminyltransferase III
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Homo sapiens

General Information

General Information Comment Organism
metabolism interplay between GnT-III and sialyltransferases in the expression of their enzymatic products and also their functions in tumor metastasis. Interplay between GnT-III and ST6GAL1 in regulating cell migration Homo sapiens
physiological function N-acetylglucosaminyltransferase III catalyzes the addition of the bisecting GlcNAc branch on N-glycans, and is a metastasis suppressor with an important role of GnT-III in N-glycan biosynthesis and tumor cell behaviours. Increased expression of GnT-III in human hepatomas, glioma, and ovarian cancers. Overexpression of GnT-III significantly inhibits alpha2,3-sialylation but not alpha2,6-sialylation via post-transcriptional mechanisms. GnT-III plays an anti-migratory role in tumor cells without or with a low level of alpha2,6-linked sialic acids but not in those alpha2,6-hypersialylated Homo sapiens