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UDP-N-acetyl-D-glucosamine + asialo-alpha1 acid glycoprotein
?
no activity
-
-
?
UDP-N-acetyl-D-glucosamine + asialo-submaxillary mucin
?
UDP-N-acetyl-D-glucosamine + asialofetuin
?
-
-
-
?
UDP-N-acetyl-D-glucosamine + asialoglycophorin A
?
best substrate
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-methylumbelliferyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-methylumbelliferyl
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-p-nitrophenyl
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
UDP-N-acetyl-D-glucosamine + fetuin
?
no activity
-
-
?
UDP-GlcNAc + (Galbeta1-3GalNAcalpha1-)TAGV
UDP + (Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TAGV
-
pH 7.0, 0.2 mM, 1250% activity
-
-
?
UDP-GlcNAc + 4-nitrophenyl 2-(acetylamino)-2-deoxy-3-O-beta-D-galactopyranosyl-alpha-D-galactopyranoside
UDP + 4-nitrophenyl 2-(acetylamino)-2-deoxy-beta-D-glucopyranosyl-(1-6)-[beta-D-galactopyranosyl-(1-3)]-2-(acetylamino)-2-deoxy-alpha-D-galactopyranoside
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-G-(Galbeta1-3GalNAcalpha1-)TTTPIST-NH2
UDP + Ac-G-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTTPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-G-(Galbeta1->3GalNAcbeta1->)TTTPIST-NH2
UDP + Ac-G-(Galbeta1->3[Glcbeta1->6]GalNAcbeta1->)TTTPIST-NH2
-
pH 7.0, 0.2 mM, 75% activity
-
-
?
UDP-GlcNAc + Ac-GT-(Galbeta1-3GalNAcalpha1-)TTPIST-NH2
UDP + Ac-GT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-GT-(Galbeta1->3GalNAcbeta1->)TTPIST-NH2
UDP + Ac-GT-(Galbeta1->3[Glcbeta1->6]GalNAcbeta1->)TTPIST-NH2
-
pH 7.0, 0.2 mM, 150% activity
-
-
?
UDP-GlcNAc + Ac-GTT-(Galbeta1-3GalNAcalpha1-)TPIST-NH2
UDP + Ac-GTT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-GTT-(Galbeta1->3GalNAcbeta1->)TPIST-NH2
UDP + Ac-GTT-(Galbeta1->3[Glcbeta1->6]GalNAcbeta1->)TPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-P-(Galbeta1-3GalNAcalpha1-)TTTGIST-NH2
UDP + Ac-P-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTTGIST-NH2
-
pH 7.0, 0.2 mM, 50% activity
-
-
?
UDP-GlcNAc + Ac-P-(Galbeta1-3GalNAcalpha1-)TTTPIST-NH2
UDP + Ac-P-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTTPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-P-(Galbeta1->3GalNAcbeta1->)TTTGIST-NH2
UDP + Ac-P-(Galbeta1->3[GlcNAcbeta1->6]GalNAcbeta1->)TTTGIST-NH2
-
pH 7.0, 0.2 mM, 200% activity
-
-
?
UDP-GlcNAc + Ac-P-(Galbeta1->3GalNAcbeta1->)TTTPIST-NH2
UDP + Ac-P-(Galbeta1->3[Glcbeta1->6]GalNAcbeta1->)TTTPIST-NH2
-
pH 7.0, 0.2 mM, 175% activity
-
-
?
UDP-GlcNAc + Ac-PT-(Galbeta1-3GalNAcalpha1-)TTGIST-NH2
UDP + Ac-PT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTGIST-NH2
-
pH 7.0, 0.2 mM, 300% activity
-
-
?
UDP-GlcNAc + Ac-PT-(Galbeta1-3GalNAcalpha1-)TTPIST-NH2
UDP + Ac-PT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTPIST-NH2
-
pH 7.0, 0.2 mM, 200% activity
-
-
?
UDP-GlcNAc + Ac-PT-(Galbeta1->3GalNAcbeta1->)TTGIST-NH2
UDP + Ac-PT-(Galbeta1->3[Glcbeta1->6]GalNAcbeta1->)TTGIST-NH2
-
pH 7.0, 0.2 mM, 95% activity
-
-
?
UDP-GlcNAc + Ac-PT-(Galbeta1->3GalNAcbeta1->)TTPIST-NH2
UDP + Ac-PT-(Galbeta1->3[GlcNAcbeta1->6]GalNAcbeta1->)TTPIST-NH2
-
pH 7.0, 0.2 mM, 185% activity
-
-
?
UDP-GlcNAc + Ac-PTT-(Galbeta1-3GalNAcalpha1-)TGIST-NH2
UDP + Ac-PTT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TGIST-NH2
-
pH 7.0, 0.2 mM, 200% activity
-
-
?
UDP-GlcNAc + Ac-PTT-(Galbeta1-3GalNAcalpha1-)TPIST-NH2
UDP + Ac-PTT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TPIST-NH2
-
pH 7.0, 0.2 mM, 100% activity
-
-
?
UDP-GlcNAc + Ac-PTT-(Galbeta1->3GalNAcbeta1->)TPIST-NH2
UDP + Ac-PTT-(Galbeta1->3[GlcNAcbeta1->6]GalNAcbeta1->)TPIST-NH2
-
pH 7.0, 0.2 mM, 10% activity
-
-
?
UDP-GlcNAc + AP-(Galbeta1-3GalNAcalpha1-)TSS
UDP + AP-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TSS
-
pH 7.0, 0.2 mM, 250% activity
-
-
?
UDP-GlcNAc + T-(Galbeta1-3GalNAcalpha1-)TTVTPTPTG
UDP + T-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TTVTPTPTG
-
pH 7.0, 0.2 mM, 75% activity
-
-
?
UDP-GlcNAc + TT-(Galbeta1-3GalNAcalpha1-)TVTPTPTG
UDP + TT-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TVTPTPTG
-
pH 7.0, 0.2 mM, 75% activity
-
-
?
UDP-GlcNAc + TTTV -(Galbeta1-3GalNAcalpha1-)TPTPTG
UDP + TTTV -(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TPTPTG
-
pH 7.0, 0.2 mM, 75% activity
-
-
?
UDP-GlcNAc + TTTVTP-(Galbeta1-3GalNAcalpha1-)TPTG
UDP + TTTVTP-(Galbeta1-3[GlcNAcbeta1-6]GalNAcalpha1-)TPTG
-
pH 7.0, 0.2 mM, 50% activity
-
-
?
UDP-N-acetyl-alpha-D-glucosamine + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl-R
-
-
-
?
UDP-N-acetyl-alpha-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-alpha-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D- galactosaminyl-benzyl
-
-
-
-
?
UDP-N-acetyl-alpha-D-glucosamine + O3-[beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl]-L-seryl/threonyl-[protein]
UDP + O3-(beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl)-L-seryl/threonyl-[protein]
-
-
-
?
UDP-N-acetyl-alpha-D-glucosamine + porcine submaxillary mucin polypeptide
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + 3-deoxy-beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + 3-deoxy-beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + 4-deoxy-beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + 4-deoxy-beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-(6-deoxy)-N-acetyl-D-galactosaminyl-benzyl
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosamine
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosamine
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-methyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-methyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-o-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-o-nitrophenyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-phenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-phenyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
UDP-N-acetyl-D-glucosamine + fucosyl-alpha-1,2-galactosyl-beta-1,3-N-acetyl-D-galactosaminyl-R
UDP + fucosyl-alpha-1,2-galactosyl-beta-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
low activity
-
-
?
UDP-N-acetyl-D-glucosamine + Galbeta(1-3)GalNAcalpha-p-nitrophenol
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + Galbeta1,3GalNAc-O-p-nitrophenyl
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + Galbeta1,3GalNAcalpha1-p-nitrophenyl
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + N-acetylgalactosaminyl-Ser(Thr)-mucin
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + submaxillary mucin polypeptide
?
-
porcine acceptor substrate
-
-
?
additional information
?
-
UDP-N-acetyl-D-glucosamine + asialo-submaxillary mucin
?
low activity
-
-
?
UDP-N-acetyl-D-glucosamine + asialo-submaxillary mucin
?
bovine asialo-submaxillary mucin
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
substrate specificity
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
i.e. core class 1, R: polypeptide
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-(6-deoxy)-N-acetyl-D-galactosaminyl-benzyl
?
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-(6-deoxy)-N-acetyl-D-galactosaminyl-benzyl
?
-
at high concentration inhibitory
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-benzyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-benzyl
-
requirement for the 4- and 6-hydroxyls of N-acetyl-galactosamine and the hydroxyl of galactose in the acceptor substrate
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-p-nitrophenyl
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-p-nitrophenyl
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-p-nitrophenyl
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-p-nitrophenyl
-
inhibitory under UV-radiation
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
-
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
-
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
-
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
substrate specificity
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
large scale preparation
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
i.e. core class 1, R: polypeptide
i.e. core class 2
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
involved in biosynthesis of O-glycans core class 2
-
-
?
UDP-N-acetyl-D-glucosamine + beta-D-galactosyl-1,3-N-acetyl-D-galactosaminyl-R
UDP + beta-D-galactosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,6)-N-acetyl-D-galactosaminyl-R
-
involved in mucin oligosaccharide biosynthesis
-
-
?
additional information
?
-
no activity human transferrin and IgG, N-acetylgalactosamine, core 3 substrates
-
-
?
additional information
?
-
no activity human transferrin and IgG, N-acetylgalactosamine, core 3 substrates
-
-
?
additional information
?
-
no activity human transferrin and IgG, N-acetylgalactosamine, core 3 substrates
-
-
?
additional information
?
-
-
no activity human transferrin and IgG, N-acetylgalactosamine, core 3 substrates
-
-
?
additional information
?
-
-
no substrate: galactosyl-beta-1,3-N-acetyl-D-galactosamine
-
-
?
additional information
?
-
-
attachment of UDPGlcNAc to serine or threonine residue
-
-
?
additional information
?
-
-
patients with Wiskott-Aldrich-Syndrome show an altered enzyme activity and inversed enzyme stimulation in T cells, enzyme activity in platelets is 3fold higher compared to normal organisms
-
-
?
additional information
?
-
-
overview: structure of O-glycans
-
-
?
additional information
?
-
-
enzyme activity is increased in patients with chronic myelogenous leukemia CML or acute myeloid leukemia AML
-
-
?
additional information
?
-
-
enzyme activity is increased in patients with chronic myelogenous leukemia CML or acute myeloid leukemia AML
-
-
?
additional information
?
-
-
M isoform is upregulated by both all-trans retinoic acid and by IL-4/13. L-isoform is moderately upregulated by IL-4/13 but not by all-trans retinoic acid
-
-
?
additional information
?
-
-
the M isoform of C2GnT can form all mucin glycan beta1,6-branched structures, including core 2, core 4, and blood group I antigen. The L-isoform forms only core 2 structures
-
-
?
additional information
?
-
-
C2GnT-1 regulates selectin ligand expression. Downregulation of the selectin ligand expression level inhibits tissue infiltration of BCP-leukemia cells
-
-
?
additional information
?
-
-
glucose levels, plasma TNF-alpha nd core 2 GlcNAc-T activity are functionally linked with dabetic retinopathy
-
-
?
additional information
?
-
-
key enzyme for the biosynthesis of sialyl-Lewis x determinants on selectin ligands
-
-
?
additional information
?
-
-
transcription of core 2 beta1,6 N-acetylglucosaminyltransferase-I is controlled by Sp1 in lymphocytes and epithelial cells
-
-
?
additional information
?
-
KRT1 binds the biotinylated CT peptide MVQWKRL of C2GnT-M isozyme
-
-
?
additional information
?
-
-
KRT1 binds the biotinylated CT peptide MVQWKRL of C2GnT-M isozyme
-
-
?
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Adenocarcinoma
Butyrate induces sLex synthesis by stimulation of selective glycosyltransferase genes.
Adenocarcinoma
Clinicopathological significance of core 2 beta1,6-N-acetylglucosaminyltransferase messenger RNA expressed in the pulmonary adenocarcinoma determined by in situ hybridization.
Adenocarcinoma
The high affinity selectin glycan ligand C2-O-sLex and mRNA transcripts of the core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT1) gene are highly expressed in human colorectal adenocarcinomas.
beta-1,3-galactosyl-o-glycosyl-glycoprotein beta-1,6-n-acetylglucosaminyltransferase deficiency
Core2 1-6-N-Glucosaminyltransferase-I Deficiency Protects Injured Arteries From Neointima Formation in ApoE-Deficient Mice.
beta-1,3-galactosyl-o-glycosyl-glycoprotein beta-1,6-n-acetylglucosaminyltransferase deficiency
Core2 1-6-N-glucosaminyltransferase-I is crucial for the formation of atherosclerotic lesions in apolipoprotein E-deficient mice.
beta-1,3-galactosyl-o-glycosyl-glycoprotein beta-1,6-n-acetylglucosaminyltransferase deficiency
Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.
beta-1,3-galactosyl-o-glycosyl-glycoprotein beta-1,6-n-acetylglucosaminyltransferase deficiency
Glycosyltransferase Function in Core 2-Type Protein O-Glycosylation.
Breast Neoplasms
The relative activities of the C2GnT1 and ST3Gal-I glycosyltransferases determine O-glycan structure and expression of a tumor-associated epitope on MUC1.
Carcinogenesis
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Carcinogenesis
Small-Molecule Inhibition of GCNT3 Disrupts Mucin Biosynthesis and Malignant Cellular Behaviors in Pancreatic Cancer.
Carcinogenesis
The role of glycosyltransferase enzyme GCNT3 in colon and ovarian cancer prognosis and chemoresistance.
Carcinoma
Biosynthesis of branched polylactosaminoglycans. Embryonal carcinoma cells express midchain beta1,6-N-acetylglucosaminyltransferase activity that generates branches to preformed linear backbones.
Carcinoma
C2-O-sLeX glycoproteins are E-selectin ligands that regulate invasion of human colon and hepatic carcinoma cells.
Carcinoma
Core 2 beta1,6-N-acetylglucosaminyltransferases and alpha1,3-fucosyltransferases regulate the synthesis of O-glycans on selectin ligands on oral cavity carcinoma cells.
Carcinoma
Expression of core 2 beta1,6-N-acetylglucosaminyltransferase facilitates prostate cancer progression.
Carcinoma
Glycosylation is an Androgen-Regulated Process Essential for Prostate Cancer Cell Viability.
Carcinoma
[Glycosyltransferase genes as tumor marker]
Carcinoma, Embryonal
Biosynthesis of branched polylactosaminoglycans. Embryonal carcinoma cells express midchain beta1,6-N-acetylglucosaminyltransferase activity that generates branches to preformed linear backbones.
Carcinoma, Non-Small-Cell Lung
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Carcinoma, Ovarian Epithelial
The role of glycosyltransferase enzyme GCNT3 in colon and ovarian cancer prognosis and chemoresistance.
Cardiomegaly
Overexpression of core 2 N-acetylglycosaminyltransferase enhances cytokine actions and induces hypertrophic myocardium in transgenic mice.
Cholera
Regulation of UDP-GlcNAc:Gal beta 1-3GalNAc-R beta 1-6-N-acetylglucosaminyltransferase (GlcNAc to GalNAc) in Chinese hamster ovary cells.
Choriocarcinoma
Core 2 ?1,6-N-acetylglucosaminyltransferases accelerate the escape of choriocarcinoma from natural killer cell immunity.
Colitis
Characterization of mice with targeted deletion of the gene encoding core 2 beta1,6-N-acetylglucosaminyltransferase-2.
Colitis
Glycosyltransferase Function in Core 2-Type Protein O-Glycosylation.
Colitis
Keratin 1 Plays a Critical Role in Golgi Localization of Core 2 N-Acetylglucosaminyltransferase M via Interaction with Its Cytoplasmic Tail.
Colonic Neoplasms
C2GnT-M is downregulated in colorectal cancer and its re-expression causes growth inhibition of colon cancer cells.
Colonic Neoplasms
Clinical relevance of the differential expression of the glycosyltransferase gene GCNT3 in colon cancer.
Colonic Neoplasms
Keratin 1 Plays a Critical Role in Golgi Localization of Core 2 N-Acetylglucosaminyltransferase M via Interaction with Its Cytoplasmic Tail.
Colonic Neoplasms
Pathways of mucin O-glycosylation in normal and malignant rat colonic epithelial cells reveal a mechanism for cancer-associated Sialyl-Tn antigen expression.
Colorectal Neoplasms
C2GnT-M is downregulated in colorectal cancer and its re-expression causes growth inhibition of colon cancer cells.
Colorectal Neoplasms
Carcinoma-associated expression of core 2 beta-1,6-N-acetylglucosaminyltransferase gene in human colorectal cancer: role of O-glycans in tumor progression.
Colorectal Neoplasms
Overexpression of sialyltransferase CMP-sialic acid:Galbeta1,3GalNAc-R alpha6-Sialyltransferase is related to poor patient survival in human colorectal carcinomas.
Colorectal Neoplasms
The role of glycosyltransferase enzyme GCNT3 in colon and ovarian cancer prognosis and chemoresistance.
Diabetes Mellitus, Type 2
Clinical validation of a link between TNF-alpha and the glycosylation enzyme core 2 GlcNAc-T and the relationship of this link to diabetic retinopathy.
Diabetic Cardiomyopathies
Overexpression of core 2 N-acetylglycosaminyltransferase enhances cytokine actions and induces hypertrophic myocardium in transgenic mice.
Diabetic Retinopathy
Clinical validation of a link between TNF-alpha and the glycosylation enzyme core 2 GlcNAc-T and the relationship of this link to diabetic retinopathy.
Diabetic Retinopathy
Protein kinase C beta2-dependent phosphorylation of core 2 GlcNAc-T promotes leukocyte-endothelial cell adhesion: a mechanism underlying capillary occlusion in diabetic retinopathy.
Diabetic Retinopathy
Tumor necrosis factor-alpha in diabetic plasma increases the activity of core 2 GlcNAc-T and adherence of human leukocytes to retinal endothelial cells: significance of core 2 GlcNAc-T in diabetic retinopathy.
Endometrial Neoplasms
Immunohistochemical expression of core 2 ?1,6-N-acetylglucosaminyl transferase 1 (C2GnT1) in endometrioid-type endometrial carcinoma: a novel potential prognostic factor.
Eosinophilia
Gene Expression Analysis by Real-Time PCR in Nasal Brushings of Adult Patients with Allergic Rhinitis, Suspected Allergic Rhinitis, and Nonallergic Rhinitis.
Gastroenteritis
Lack of functional P-selectin ligand exacerbates Salmonella serovar typhimurium infection.
Gestational Trophoblastic Disease
Core 2 ?1,6-N-acetylglucosaminyltransferases accelerate the escape of choriocarcinoma from natural killer cell immunity.
Graft vs Host Disease
GCNT1-Mediated O-Glycosylation of the Sialomucin CD43 Is a Sensitive Indicator of Notch Signaling in Activated T Cells.
Hyperglycemia
Identification and characterization of a gene regulating enzymatic glycosylation which is induced by diabetes and hyperglycemia specifically in rat cardiac tissue.
Immune System Diseases
In vivo overexpression of Core2 N-acetylglucosaminyltransferase prevents repopulation of the bone marrow with colony forming cells but fails to affect normal T cell development.
Infections
Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.
Infections
Lack of functional P-selectin ligand exacerbates Salmonella serovar typhimurium infection.
Infections
Mucin biosynthesis in the bovine goblet cell induced by Cooperia oncophora infection.
Infections
N-Acetylcysteine supplementation alleviates intestinal injury in piglets infected by porcine epidemic diarrhea virus.
Leukemia
Processing O-glycan core 1, Gal beta 1-3GalNAc alpha-R. Specificities of core 2, UDP-GlcNAc: Gal beta 1-3 GalNAc-R(GlcNAc to GalNAc) beta 6-N-acetylglucosaminyltransferase and CMP-sialic acid: Gal beta 1-3GalNAc-R alpha 3-sialyltransferase.
Leukemia
Transfection of antisense core 2 beta1,6-N-acetylglucosaminyltransferase-1 cDNA suppresses selectin ligand expression and tissue infiltration of B-cell precursor leukemia cells.
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Biosynthesis of O-glycans in leukocytes from normal donors and from patients with leukemia: increase in O-glycan core 2 UDP-GlcNAc:Gal beta 3 GalNAc alpha-R (GlcNAc to GalNAc) beta(1-6)-N-acetylglucosaminyltransferase in leukemic cells.
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Processing O-glycan core 1, Gal beta 1-3GalNAc alpha-R. Specificities of core 2, UDP-GlcNAc: Gal beta 1-3 GalNAc-R(GlcNAc to GalNAc) beta 6-N-acetylglucosaminyltransferase and CMP-sialic acid: Gal beta 1-3GalNAc-R alpha 3-sialyltransferase.
Leukemia, Myeloid, Acute
Processing O-glycan core 1, Gal beta 1-3GalNAc alpha-R. Specificities of core 2, UDP-GlcNAc: Gal beta 1-3 GalNAc-R(GlcNAc to GalNAc) beta 6-N-acetylglucosaminyltransferase and CMP-sialic acid: Gal beta 1-3GalNAc-R alpha 3-sialyltransferase.
Lung Neoplasms
Clinicopathological significance of core 2 beta1,6-N-acetylglucosaminyltransferase messenger RNA expressed in the pulmonary adenocarcinoma determined by in situ hybridization.
Lung Neoplasms
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Lung Neoplasms
[Glycosyltransferase genes as tumor marker]
Lymphatic Metastasis
Clinicopathological significance of core 2 beta1,6-N-acetylglucosaminyltransferase messenger RNA expressed in the pulmonary adenocarcinoma determined by in situ hybridization.
Lymphatic Metastasis
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Lymphoma
Haploinsufficiency of C2GnT-I glycosyltransferase renders T lymphoma cells resistant to cell death.
Melanoma
ß-1,3-galactosyl-O-glycosyl-glycoprotein ß-1,6-N-acetylglucosaminyltransferase 3 Increases MCAM Stability, Which Enhances S100A8/A9-Mediated Cancer Motility.
Neoplasm Metastasis
Aberrant Glycosylation Promotes Lung Cancer Metastasis through Adhesion to Galectins in the Metastatic Niche.
Neoplasm Metastasis
Clinicopathological significance of core 2 beta1,6-N-acetylglucosaminyltransferase messenger RNA expressed in the pulmonary adenocarcinoma determined by in situ hybridization.
Neoplasm Metastasis
Core 2 beta1,6-N-acetylglucosaminyltransferases and alpha1,3-fucosyltransferases regulate the synthesis of O-glycans on selectin ligands on oral cavity carcinoma cells.
Neoplasm Metastasis
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Neoplasm Metastasis
Global analysis of human glycosyltransferases reveals novel targets for pancreatic cancer pathogenesis.
Neoplasm Metastasis
Golgi phosphoprotein 3 determines cell binding properties under dynamic flow by controlling Golgi localization of core 2 N-acetylglucosaminyltransferase 1.
Neoplasm Metastasis
MiR-BART1-5p targets core 2?-1,6-acetylglucosaminyltransferase GCNT3 to inhibit cell proliferation and migration in EBV-associated gastric cancer.
Neoplasm Metastasis
TGF-?1 Causes EMT by regulating N-Acetyl Glucosaminyl Transferases via Downregulation of Non Muscle Myosin II-A through JNK/P38/PI3K pathway in lung cancer.
Neoplasms
Aberrant Glycosylation Promotes Lung Cancer Metastasis through Adhesion to Galectins in the Metastatic Niche.
Neoplasms
C2GnT-M is downregulated in colorectal cancer and its re-expression causes growth inhibition of colon cancer cells.
Neoplasms
Carcinoma-associated expression of core 2 beta-1,6-N-acetylglucosaminyltransferase gene in human colorectal cancer: role of O-glycans in tumor progression.
Neoplasms
Cellular crosstalk between TNF-?, NADPH oxidase, PKC?2, and C2GNT in human leukocytes.
Neoplasms
Clinical relevance of the differential expression of the glycosyltransferase gene GCNT3 in colon cancer.
Neoplasms
Core 2 ?-1, 6-N-acetylglucosaminyltransferase-1 expression in prostate biopsy specimen is an indicator of prostate cancer aggressiveness.
Neoplasms
Core 2 ?1,6-N-acetylglucosaminyltransferases accelerate the escape of choriocarcinoma from natural killer cell immunity.
Neoplasms
Core 2 N-acetylglucosaminyltransferase-1 expression induces aggressive potential of testicular germ cell tumor.
Neoplasms
Downregulation of N-Acetylglucosaminyltransferase GCNT3 by miR-302b-3p Decreases Non-Small Cell Lung Cancer (NSCLC) Cell Proliferation, Migration and Invasion.
Neoplasms
Expression of core 2 beta1,6-N-acetylglucosaminyltransferase facilitates prostate cancer progression.
Neoplasms
GCNT4 is Associated with Prognosis and Suppress Cell Proliferation in Gastric Cancer.
Neoplasms
Golgi phosphoprotein 3 determines cell binding properties under dynamic flow by controlling Golgi localization of core 2 N-acetylglucosaminyltransferase 1.
Neoplasms
In vivo overexpression of Core2 N-acetylglucosaminyltransferase prevents repopulation of the bone marrow with colony forming cells but fails to affect normal T cell development.
Neoplasms
MiR-BART1-5p targets core 2?-1,6-acetylglucosaminyltransferase GCNT3 to inhibit cell proliferation and migration in EBV-associated gastric cancer.
Neoplasms
Molecular Pathways: Mucins and Drug Delivery in Cancer.
Neoplasms
MUC1 carrying core 2 O-glycans functions as a molecular shield against NK cell attack, promoting bladder tumor metastasis.
Neoplasms
Pancreas carcinoma antigen fused to invariant chain elicits T-cell response and tumor growth inhibition.
Neoplasms
Pseudomonas aeruginosa pyocyanin modulates mucin glycosylation with sialyl-Lewis(x) to increase binding to airway epithelial cells.
Neoplasms
Recent progress and perspectives on prostate cancer biomarkers.
Neoplasms
Restoration of compact Golgi morphology in advanced prostate cancer enhances susceptibility to galectin-1-induced apoptosis by modifying mucin O-glycan synthesis.
Neoplasms
Small-Molecule Inhibition of GCNT3 Disrupts Mucin Biosynthesis and Malignant Cellular Behaviors in Pancreatic Cancer.
Neoplasms
The high affinity selectin glycan ligand C2-O-sLex and mRNA transcripts of the core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT1) gene are highly expressed in human colorectal adenocarcinomas.
Neoplasms
The relative activities of the C2GnT1 and ST3Gal-I glycosyltransferases determine O-glycan structure and expression of a tumor-associated epitope on MUC1.
Neoplasms
The transcriptional profiling of glycogenes associated with hepatocellular carcinoma metastasis.
Neoplasms
Tumor initiating but differentiated luminal-like breast cancer cells are highly invasive in the absence of basal-like activity.
Neoplasms
Tumor necrosis factor-alpha in diabetic plasma increases the activity of core 2 GlcNAc-T and adherence of human leukocytes to retinal endothelial cells: significance of core 2 GlcNAc-T in diabetic retinopathy.
Neoplasms
Whole-transcriptome sequencing identified gene expression signatures associated with aggressive clear cell renal cell carcinoma.
Neoplasms
[Glycosyltransferase genes as tumor marker]
Neoplasms, Germ Cell and Embryonal
Core 2 N-acetylglucosaminyltransferase-1 expression induces aggressive potential of testicular germ cell tumor.
Neoplastic Cells, Circulating
Recent progress and perspectives on prostate cancer biomarkers.
Ovarian Neoplasms
The role of glycosyltransferase enzyme GCNT3 in colon and ovarian cancer prognosis and chemoresistance.
Pancreatic Neoplasms
Expression of core 2 beta-1,6-N-acetylglucosaminyltransferase in a human pancreatic cancer cell line results in altered expression of MUC1 tumor-associated epitopes.
Pancreatic Neoplasms
Expression of microRNA-15b and the glycosyltransferase GCNT3 correlates with antitumor efficacy of Rosemary diterpenes in colon and pancreatic cancer.
Pancreatic Neoplasms
Pancreas carcinoma antigen fused to invariant chain elicits T-cell response and tumor growth inhibition.
Pancreatic Neoplasms
Small-Molecule Inhibition of GCNT3 Disrupts Mucin Biosynthesis and Malignant Cellular Behaviors in Pancreatic Cancer.
Prostatic Hyperplasia
An A/G polymorphism of core 2 branching enzyme gene is associated with prostate cancer.
Prostatic Neoplasms
An A/G polymorphism of core 2 branching enzyme gene is associated with prostate cancer.
Prostatic Neoplasms
Core2 O-glycan-expressing prostate cancer cells are resistant to NK cell immunity.
Prostatic Neoplasms
Determination of carbohydrate structure recognized by prostate-specific F77 monoclonal antibody through expression analysis of glycosyltransferase genes.
Prostatic Neoplasms
Expression of core 2 beta1,6-N-acetylglucosaminyltransferase facilitates prostate cancer progression.
Prostatic Neoplasms
Glycosylation is a global target for androgen control in prostate cancer cells.
Prostatic Neoplasms
Increased expression of GCNT1 is associated with altered O-glycosylation of PSA, PAP, and MUC1 in human prostate cancers.
Prostatic Neoplasms
Restoration of compact Golgi morphology in advanced prostate cancer enhances susceptibility to galectin-1-induced apoptosis by modifying mucin O-glycan synthesis.
Prostatic Neoplasms
The androgen receptor controls expression of the cancer-associated sTn antigen and cell adhesion through induction of ST6GalNAc1 in prostate cancer.
Rhinitis, Allergic
Gene Expression Analysis by Real-Time PCR in Nasal Brushings of Adult Patients with Allergic Rhinitis, Suspected Allergic Rhinitis, and Nonallergic Rhinitis.
Stomach Neoplasms
Epstein-Barr Virus-Encoded Latent Membrane Protein 2A Downregulates GCNT3 via the TGF-?1/Smad-mTORC1 Signaling Axis.
Stomach Neoplasms
GCNT4 is Associated with Prognosis and Suppress Cell Proliferation in Gastric Cancer.
Stomach Neoplasms
MiR-BART1-5p targets core 2?-1,6-acetylglucosaminyltransferase GCNT3 to inhibit cell proliferation and migration in EBV-associated gastric cancer.
Stroke
Smoking affects gene expression in blood of patients with ischemic stroke.
Tuberculosis
Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.
Urinary Bladder Neoplasms
A mechanism for evasion of CTL immunity by altered O-glycosylation of HLA class I.
Urinary Bladder Neoplasms
A novel strategy for evasion of NK cell immunity by tumours expressing core2 O-glycans.
Urinary Bladder Neoplasms
MUC1 carrying core 2 O-glycans functions as a molecular shield against NK cell attack, promoting bladder tumor metastasis.
Wiskott-Aldrich Syndrome
Branched O-linked oligosaccharides ectopically expressed in transgenic mice reduce primary T-cell immune responses.
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peripheral blood
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low content
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high content
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an EBVnGC cell line
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an EBVnGC cell line
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GCNT3 is elevated in skin and mesothelioma cells and in some lung and breast cancer cells
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differential expression of GCNT3 gene among tumour samples from stage II colon cancer patients by quantitative reverse-transcription PCR, overview
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GCNT3 gene expression is downregulated in colorectal cancer (CRC) samples in comparison to non-pathological colon tissue
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maturation of dendritic cells leads to a rapid change in the expression of glycosyltransferases involved in O-linked glycosylation. A down-regulation of C2GnT1 mRNA and enzymatic activity is observed with a concurrent up-regulation of ST3Gal I and ST6GalNAc II mRNA resulting in a loss of the core 2 structures required for sLex expression as a P-selectin ligand
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expression of C2GnT1 in 84 cases of endometrioid-type endometrial carcinoma, 15 cases of endometrial hyperplasia, and 30 normal endometria, immunohistochemic analysis, overview. C2GnT1 is strongly expressed at the invasive tumour front in several cases
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GCNT3 expression analysis in a cohort of 56 EOC patients, followed by a meta-analysis of more than one thousand patients, overview
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GCNT3 expression in Epstein-Barr virus (EBV)-associated gastric cancer cells and tissues is lower than in EBV-negative gastric cancer cells (EBVnGC) and tissues, and high expression is significantly associated with advanced tumor-lymph node metastasis. GCNT3 is closely related to the ERK signaling pathway and epithelial mesenchymal transition (EMT), regulating cell proliferation, migration, and invasion
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an EBVaGC cell line
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an EBVaGC cell line
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an EBVnGC cell line
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NCI498, ileo-caecal carcinoma cell line
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transcription of core 2 beta1,6 N-acetylglucosaminyltransferase-I is controlled by Sp1 in lymphocytes and epithelial cells
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erythroleukemia cell line
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pre-B lymphocytic leukemia cell line
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colonic adenocarcinoma cell line
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YC2C2 lymphocytic leukemia cell line
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GCNT3 is overexpressed in highly metastatic melanomas
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GCNT3 is highly expressed in both NSCLC tissues and cell lines
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an EBVnGC cell line
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an EBVaGC cell line
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colonic grade II tumour cell line
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colonic grade III tumour cell line
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colonic large ulcerating grade IV tumour cell line, low activity
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acute myeloid leukemia blast cell line
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18fold increased level compared to normal granulocytes
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chronic myelogenous leukemia granulocyte cell line
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4fold increased level compared to normal granulocytes
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colonic adenocarcinoma cell line
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high levels of endogenous GCNT3
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core 2 N-acetylglucosaminyltransferase is downregulated in galectin-1-resistant PSA-LNCaP cells compared with galectin-1-sensitive PSA+ LNCaP cells
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airway epithelial cell line
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transcription of core 2 beta1,6 N-acetylglucosaminyltransferase-I is controlled by Sp1 in lymphocytes and epithelial cells
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core2GnT and core 2-branched O-glycans synthesized play a critical role in prostate cancer progression. Core2GnT in prostate carcinoma cells facilitates adhesion to type IV collagen and laminin, and this increased adhesion may be a cause for aggressive tumor formation by prostate cancer cells expressing core2GnT
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GCNT1 immunohistochemic analysis, overview. The anti-GCNT1 monoclonal antibody shows high specificity against human GCNT1
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additional information
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additional information
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not in breast cancer cell lines
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additional information
human pancreatic cancer tissue array consisting of 90 cases of tumor and matched normal adjacent tissue with survival data, overview
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human pancreatic cancer tissue array consisting of 90 cases of tumor and matched normal adjacent tissue with survival data, overview
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additional information
the isozyme is distributed in mucin-secreting tissues along the gastrointestinal tract
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the isozyme is distributed in mucin-secreting tissues along the gastrointestinal tract
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additional information
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topologically, C2GnT1 is strongly expressed at sites of deep myometrial invasion
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additional information
GCNT3 is highly expressed in both NSCLC tissues and cell lines, and higher expression is significantly associated with advanced tumor lymph node metastasis (TNM) stage, positive lymph node metastasis, and poor overall survival. GCNT3 expression is associated with lymph node metastasis and age. But the expression level of GCNT3 is not correlated with gender, tumor location, differentiation grade, etc.. Expression of GCNT3 is lower in EBVaGC cells and tissues than that in EBVnGC cells and tissues
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GCNT3 is highly expressed in both NSCLC tissues and cell lines, and higher expression is significantly associated with advanced tumor lymph node metastasis (TNM) stage, positive lymph node metastasis, and poor overall survival. GCNT3 expression is associated with lymph node metastasis and age. But the expression level of GCNT3 is not correlated with gender, tumor location, differentiation grade, etc.. Expression of GCNT3 is lower in EBVaGC cells and tissues than that in EBVnGC cells and tissues
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additional information
integrated transcriptomic and proteomic analyses reveal that GCNT3 is linked to cellular cycle, mitosis and proliferation. The non-invasive HT-29 cell line, that is isolated from a primary tumor, shows GCNT3 expression (mRNA and protein). By contrast, cells belonging to metastatic and invasive SW family, e.g. SW620 and SW5FU, do not exhibit measurable GCNT3 expression
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integrated transcriptomic and proteomic analyses reveal that GCNT3 is linked to cellular cycle, mitosis and proliferation. The non-invasive HT-29 cell line, that is isolated from a primary tumor, shows GCNT3 expression (mRNA and protein). By contrast, cells belonging to metastatic and invasive SW family, e.g. SW620 and SW5FU, do not exhibit measurable GCNT3 expression
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quantitative RT-PCR expression analysis
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quantitative RT-PCR expression analysis
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STAT4 controls Gcnt1 expression in Th1 cells, several several conserved and non-conserved predicted STAT4 binding sites are determined. Functional importance of STAT4 for P-lig induction and specifically on the enhancer as a transactivating factor. Prolonged T-bet binding to the Gcnt1 enhancer
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malfunction
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higher presence of the enzyme in higher stages of testicular germ cell tumors, promotes aggressive behavior of cancer cells
malfunction
aberrant GCNT3 expression is associated with increased mucin production, aggressive tumorigenesis, and reduced patient survival, and CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells reduces proliferation and spheroid formation. Inhibitor talniflumate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro
malfunction
GCNT1-overexpressing cells produce a significantly larger amount of growth factors when cocultured with prostate stromal cells compared with GCNT1-knocked down cells and form larger tumors
malfunction
loss of C2GnT-M leads to development of colitis and colon cancer. Knockdown of KRT1 by siRNA does not affect Golgi morphology but leaves C2GnT-M outside of the Golgi, resulting in the formation of sialyl-T antigen
malfunction
Gcnt1-/-Th1 cells lacking C2-GlcNAcT-I expression show impaired P-lig expression similar to Fut4+7-/-Th1 cells. In contrast to impaired P-lig expression,Gcnt1-/-and Fut4 +7-/- maintain their inflammatory competence as assessed by IFNgamma expression. Functional relevance of Gcnt1 deficiency in CD4+T cells in vivo. In line with a lack of Gcnt1 transcription, naive T cells exhibit a closed histone configuration with lowH3K4me2 and prominent H3K27me3 marks. The active H3K4me2 mark in this region increases in a time-dependent manner during Th1 differentiation
malfunction
GCNT3 overexpression reduces 5-fluorouracil resistance in colorectal cancer (CRC) cells. GCNT3 overexpression reduces proliferation, invasion and changes metabolic capacities of CRC cells. The enzyme's overexpression in epithelial ovarian cancer (EOC) patients is associated with better clinical outcome and response to initial therapy
malfunction
miR-BART1-5p directly targets GCNT3. In addition, miR-BART1-5p mimics transfection is observed to reduce cell proliferation and migration, while miR-BART1-5p inhibitor increases cell proliferation and migration following transfection. In conclusion, both miR-BART1-5p and knockdown of GCNT3 inhibit cell proliferation and migration
malfunction
silencing and functional inhibition of GCNT3 greatly suppresses migration and invasion of melanoma cells, resulting in the loss of S100A8/A9 responsiveness. siRNA-mediated GCNT3 suppression and talniflumate-mediated GCNT3 suppression significantly attenuate the basal ability of in vitro migration of WM-266-4 cells
metabolism
O-glycan biosynthesis pathways and proposed O-glycan structures of selected glycosyltransferases, overview. Core 1 dominates the O-glycan repertoire. Core 1 can be further elongated by extended C1 beta3GnT3 enzyme, EC 2.4.1.146, to form extended core 1 structure, or be modified by C2 beta6GnT1 enzyme to form core 2 O-glycans. Three core 2 enzymes, C2 beta6GnT1, 2, and 3, are responsible for biosynthesis of core 2 O-glycans. C2 beta6GnT1 and 3 are almost exclusively responsible for biosynthesis of the core 2 branch, while C2 beta6GnT2 shows a significant core 4 and I-branching activity. Regulation of O-glycan biosynthesis, overview
metabolism
the enzyme is involved in the biosynthetic pathways for core2 O-glycans, overview. The core1 structure is converted to branched core2 structure (Core2) by GCNT1, GCNT3, and GCNT4
metabolism
as all fucosyltransferases 8 (FUT8), GnT-III, GnT-IV, and GnT-V use GlcNAc terminated bi-antennary glycan as acceptor substrate, the interplay among these enzymes determines the forms of glycans, e.g. the bisecting modification by GnT-III makes the glycan no longer a substrate for FUT8 and GnT-V
metabolism
integrated transcriptomic and proteomic analyses reveal that GCNT3 is linked to cellular cycle, mitosis and proliferation, response to drugs and metabolism pathways. The vascular epithelial growth factor A (VEGFA) arises as an attractive partner of GCNT3 functions in cell invasion and resistance
physiological function
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C2GnT1 synthesizes the core 2 branching structure by catalysing the transfer of GlcNAc from UDP-GlcNAc with a beta1,6-linkage to GalNAc of the core 1 chain. On this core 2 branch, several tumour-associated carbohydrate structures, such as sLex and sLea, are synthesized. The enzyme may be associated with the biological aggressiveness of tumour cells, relationship between the expression of C2GnT1 and clinicopathological parameters of patients with endometrial carcinoma, overview
physiological function
core 2 beta-1, 6-N-acetylglucosaminyltransferase-1 (GCNT1) is a key enzyme that forms core 2 branched O-glycans. GCNT1 expression is correlated with D'Amico's recurrence risk classification. GCNT1-negative tumors are associated with significantly better prostate-specific antigen (PSA)-free survival compared with GCNT1-positive tumors. GCNT1 expression status is an independent risk factor for PSA recurrence after radical prostatectomy
physiological function
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enzyme GCNT1 expression in prostate cancer specimens from radical prostatectomy correlates with prostate cancer aggressiveness
physiological function
mucin-type isozyme core 2 N-acetylglucosaminyltransferase 2/M synthesizes all three beta6GlcNAc branch structures found in secreted mucins
physiological function
the isozyme shows tumour suppressor properties, together with a role of mucin production in chemotherapy sensitivity in pancreatic cancer
physiological function
the mucin-synthesizing core 2 beta-1,6 N-acetylglucosaminyltransferase (GCNT3/C2GNT) plays a significant role in mucin biosynthesis. Correlation between GCNT3 expression and patient survival in human pancreatic cancer
physiological function
beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3 (GCNT3) is a glycosyltransferase that transfers GlcNAc to N-acetylgalactosamine (GalNAc) of the core 1 acceptor structure to form the core 2 branch in the beta-1,6 linkage. In addition to the formation of the core 2 structure, GCNT3 also functions to form the core 4 structure. GCNT3 increases MCAM stability, which enhances S100A8/A9-mediated cancer motility. Among the novel S100A8/A9 receptors, GCNT3 favorably glycosylates the MCAM receptor, extending its half-life and leading to further elevation of S100A8/A9-mediated cellular motility in melanoma cells. GCNT3 plays a pivotal role in the maintenance of MCAM protein at a high level, resulting in the acquisition of strong responsiveness to S100A8/A9 that is linked to increased cellular migration and invasion. GCNT3 expression is positively correlated to MCAM expression in patients with high-grade melanomas. GCNT3 is an upstream regulator of MCAM protein. GCNT3 plays a key role in S100A8/A9-mediated cancer motility. GCNT3 controls MCAM stability by its catalytic activity-mediated glycosyl modification that correlates with a greater ability for cancer cell motility and invasion in response to extracellular S100A8/A9
physiological function
core 2 beta1,6-N-acetylglucosaminyltransferase-I (C2GlcNAcT-I) is crucial for inflammatory homing of Th1 cells to the skin in vivo, analysis of molecular regulation of the enzyme encoded by gene Gcnt1 in CD4+T helper cells, overview. C2-GlcNAcT-I, encoded by Gcnt1, is essential for generation of P-lig and recruitment of Th1 cells into a skin-DTH reaction. Gcnt1 transcription and subsequent P-lig induction in Th1 cells is governed by binding of STAT4 and T-bet to a distal enhancer and further regulated by epigenetic marks such as H3K27me3. T-cells cultured in vitro under Th1 conditions, i.e. supplemented with IL-12, IFN gamma, and anti-IL-4, but not under Th2 (IL-4, anti-IL-12, anti-IFN gamma) or Th0 (anti-12, anti-IFNgamma and anti-IL-4) conditions, express P-lig, which corresponds to differential Gcnt1 but not Fut7 mRNA expression. STAT4 controls Gcnt1 expression in Th1 cells, several several conserved and non-conserved predicted STAT4 binding sites are determined. Functional importance of STAT4 for P-lig induction and specifically on the enhancer as a transactivating factor. Prolonged T-bet binding to the Gcnt1 enhancer
physiological function
O-glycan synthase glucosamine (N-acetyl) transferase 3 (GCNT3) is a mucin-type responsible for catalyzing core 2 and core 4 O-glycans and forming O-linked glycosylation in protein biosynthesis. Abnormal expression of GCNT3 promotes the progression of several human cancers. GCNT3 expression in Epstein-Barr virus (EBV)-associated gastric cancer cells and tissues is lower than in EBV-negative gastric cancer cells and tissues, and high expression is significantly associated with advanced tumor-lymph node metastasis. EBV may regulate GCNT3 by affecting the NF-kappaB signaling pathway. Patients with EBV-associated gastric cancer (EBVaGC) have a good survival rate. EBV potentially regulates GCNT3 by affecting the NF-kappaB signaling pathway
physiological function
the mucin-type core 2 1,6-N-acetylglucosaminyltransferase enzyme (C2GnT-M), encoded by the GCNT3 gene, is a glycosyltransferase enzyme whose expression is altered in cancer processes. GCNT3 catalyzes the formation of core 2 O-glycan, core 4 O-glycan and I branches and its pattern of expression is mainly associated with colorectal cancer (CRC) prognosis. GCNT3 transfection in certain CRC cells reduces cell proliferation, adhesion, invasion, and induced cell death, and also inhibits tumor growth in vivo. Role of glycosyltransferase enzyme GCNT3 in colon and ovarian cancer prognosis and chemoresistance, overview. Integrated transcriptomic and proteomic analyses reveal that GCNT3 is linked to cellular cycle, mitosis and proliferation, response to drugs and metabolism pathways. GCNT3 overexpression contributes to reduce 5-fluorouracil resistance in metastatic CRC cells. GCNT3 also diminishes cell invasion and VEGFA expression in EOC cells. GCNT3 is a cancer prognostic factor. GCNT3 diminishes cell proliferation, invasion and alters metabolic properties of CRC cells. GCNT3 high-expressing Stage III-IV EOC patients have better response to conventional treatment and clinical outcome
additional information
Keratin 1 retains C2GnT-M in the Golgi by interacting with its cytoplasmic tail via the rod domain. Keratin 1 plays a critical role in the regulation of O-glycosylation pathways
additional information
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Keratin 1 retains C2GnT-M in the Golgi by interacting with its cytoplasmic tail via the rod domain. Keratin 1 plays a critical role in the regulation of O-glycosylation pathways
additional information
no effect of core fucosylation of substrate on the glycosyltransferase activity of GnT-III, overview
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