2.4.1.102: beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase
This is an abbreviated version!
For detailed information about beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase, go to the full flat file.
Word Map on EC 2.4.1.102
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2.4.1.102
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o-glycans
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glycosyltransferases
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sialylated
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p-selectin
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o-linked
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selectins
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ligand-1
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core-2
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psgl-1
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fuct-vii
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st3gals
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medicine
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poly-n-acetyllactosamine
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sialyl-lewis
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udp-glcnac:gal
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diagnostics
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1-3galnac-r
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polylactosamine
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alpha2,3-sialyltransferase
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molecular biology
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synthesis
- 2.4.1.102
- o-glycans
- glycosyltransferases
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sialylated
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p-selectin
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o-linked
- selectins
- ligand-1
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core-2
- psgl-1
- fuct-vii
- st3gals
- medicine
- poly-n-acetyllactosamine
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sialyl-lewis
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udp-glcnac:gal
- diagnostics
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1-3galnac-r
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polylactosamine
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alpha2,3-sialyltransferase
- molecular biology
- synthesis
Reaction
Synonyms
2beta-1,6-acetylglucosaminyltransferase, acetylglucosaminyltransferase, uridine diphosphoacetylglucosamine-mucin beta-(1-6)-, acetylglucosaminyltransferase, uridine diphosphoacetylglucosamine-mucin beta-(1-6)-, A, bC2GnT-M, beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3, beta-1,6-N-acetylglucosaminyltransferase, beta1,6-N-acetylglucosaminyltransferase, beta6-N-acetylglucosaminyltransferase, Bo17, C2 beta6GnT1, C2/4GnT, C24GNT, C2GlcNAcT-I, C2GlcNAcT-II, C2GlcNAcT-III, C2GnT, C2GnT-1, C2GnT-I, C2GnT-L, c2GnT-M, C2GnT1, C2GnT2, C2GnT3, C2GNTM, C4GnT, core 2 acetylglucosaminyltransferase, core 2 beta-1, 6-N-acetylglucosaminyltransferase-1, core 2 beta-1,6 N-acetylglucosaminyltransferase, core 2 beta-1,6-N-acetylglucosaminyltransferase, core 2 beta1,6 N-acetylglucosaminyltransferase, core 2 beta1,6 N-acetylglucosaminyltransferase-I, core 2 beta1,6-N-acetyl-glycosaminyltransferase, core 2 beta1,6-N-acetylglucosaminyl transferase 1, core 2 beta1,6-N-acetylglucosaminyltransferase, core 2 beta1,6-N-acetylglucosaminyltransferase I, core 2 beta1,6-N-acetylglucosaminyltransferase-I, core 2 beta6-GlcNAc-transferase, core 2 beta6-N-acetylglucosaminyltransferase, core 2 GlcNAc-T, core 2 N-acetylglucosaminyltransferase, Core 2 N-acetylglucosaminyltransferase 2/M, core 2 N-acetylglucosaminyltransferase M, core 2 N-acetylglucosaminyltransferase-1, core 2 N-acetylglucosaminyltransferase-M, core 2 protein beta-1,6-N-acetylglucosaminyltransferase-mucin type, core 2beta 1,6 N-acetylglucosaminyltransferase, core 2beta-1,6-acetylglucosaminyltransferase, core 6-beta-GlcNAc-T, core 6-beta-GlcNAc-transferase A, core2 1-6-N-glucosaminyltransferase-I, core2 beta(1,6)-N-acetyglucosaminyltransferase-I, core2 beta-1,6-N-acetylglucosaminyltransferase, core2 beta-1,6-N-acetylglucosaminyltransferase-1, Core2beta1,6GnT type M, core2GnT, GCNT1, gcnt3, gcnt4, GnT-III, GNTM, More, mucin-type core 2 1,6-N-acetylglucosaminyltransferase enzyme, mucus-type core 2 beta1,6 N-acetylglucosaminyltransferase, O-glycosyl-oligosaccharide-glycoprotein N-acetylglucosaminyltransferase I, uridine diphosphoacetylglucosamine-mucin beta-(1-6)-acetylglucosaminyltransferase, uridine diphosphoacetylglucosamine-mucin beta-(1-6)-acetylglucosaminyltransferase A
ECTree
2.4.1.102 beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferaseAdvanced search results
results (
results (Engineering
Engineering on EC 2.4.1.102 - beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
C217S
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mutant enzyme with 41% of wild-type activity. Similar Km and Vmax values for Galbeta(1-3)GalNAcalpha-p-nitrophenol, Km-value for UDP-N-acetyl-D-glucosamine is 2.9fold higher than wild-type value. In contrast to wild-type enzyme, the mutant enzyme is not inhibited by sulfhydryl reagents and is not stimulated by reducing agents
T60A
T60A/T97A
T97A
C217S
S158C
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mutation reduces C2GnT activity but does not affect substrate specificity or enzyme dimerization. Mutation appears to result in haploinsufficiency of C2GnT activity. C2GnT-I haploinsufficiency is sufficient for loss of core 2 O-glycan expression and galectin-1 resistance
additional information
T60A
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about 65% of the wild-type in vitro activity, mutation results in a significant increase in electrophoretic mobilities of the protein
T60A/T97A
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about 6% of the wild-type in vitro activity, mutant loses the ability of branching P-selectin glycoprotein ligand-1 O-glycans
T97A
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about 25% of the wild-type in vitro activity, mutation results in a significant increase in electrophoretic mobilities of the protein
C217S
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Cys217 although not required for activity per se, represents the only thiol that causes enzyme inactivation when modified. KM-value for UDP-N-acetyl-D-glucosamine is about 5% higher than the wild-type value, the Km-value for Galbeta(1-3)GalNAcalpha-p-nitrophenol is about 20% higher than the wild-type value.Unlike the wild-type enzyme the mutant enzyme can be stored at 4°C for at least 3 months without any loss of activity. The mutant enzyme is insensitive to DTNB, iodoacetamide, NEM, HgCl2 and ZnCl2
additional information
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production of BoHV-4 Bo17 mutant strains, i.e. the BoHV-4 V.test strain deleted for the Bo17 ORF (Bo17 Del) and the corresponding revertant strain (Bo17 Rev). The recombinant strains Bo17 MuDir and Bo17 Spliced are derived from a cloned BoHV-4 bacterial artificial chromosome (BAC). The Bo17 MuDir sequence is generated by site-directed mutagenesis, two mutations are inserted in the 5' splice site and one mutation in the 3' splice site. O-Glycomic profile analysis of wild-type and mutant strains. The Bo17 knockout strain does not display any growth deficit in vitro. Analysis of the structures of O-glycans isolated from cells mock infected or infected with the Bo17 Del, Bo17 MuDir, Bo17 MuDir Rev, Bo17 Spliced, and Bo17 Spliced Rev strains of BoHV-4. The infection by wild-type, Bo17 MuDir, and the revertant strains is moderately inhibited by jacalin, this neutralization is significantly stronger for the Bo17 Del strain and even more for the Bo17 Spliced strain
additional information
construction of a catalytic dead GCNT3 (mutGCNT3) cDNA designed for expression as C-terminally 3xMyc-6His-tagged deletion form (lacking the region from 323 aa through 438 aa). siRNA-mediated GCNT3 suppression in WM-266-4 cells. Forced expression of mutGCNT3 significantly downregulates migration activity of WM-266-4 cells under either the presence or absence of S100A8/A9 in culture
additional information
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construction of a catalytic dead GCNT3 (mutGCNT3) cDNA designed for expression as C-terminally 3xMyc-6His-tagged deletion form (lacking the region from 323 aa through 438 aa). siRNA-mediated GCNT3 suppression in WM-266-4 cells. Forced expression of mutGCNT3 significantly downregulates migration activity of WM-266-4 cells under either the presence or absence of S100A8/A9 in culture
additional information
GCNT3 downregulation by shGCNT3 7. GCNT3 overexpression reduces 5-fluorouracil resistance in colorectal cancer (CRC) cells. GCNT3 overexpression reduces proliferation, invasion and changes metabolic capacities of CRC cells. Genomic analysis of GCNT3 overexpression, overview
additional information
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GCNT3 downregulation by shGCNT3 7. GCNT3 overexpression reduces 5-fluorouracil resistance in colorectal cancer (CRC) cells. GCNT3 overexpression reduces proliferation, invasion and changes metabolic capacities of CRC cells. Genomic analysis of GCNT3 overexpression, overview
additional information
knockdown of GCNT3 using GCNT3-specific small interfering RNAs: siGCNT3-1 (GCUACUGCGAGCUGUGUAUTT), and siGCNT3-2 (GCUCAGUGCCGUGGAAAUATT). Reduction of the expression of endogenous GCNT3 by siRNA transfection in SGC7901 and BGC823 cells. Epstein-Barr virus (EBV) miRNA miR-BART1-5p specifically targets GCNT3. miR-BART1-5p suppresses GCNT3 expression, cell proliferation, and migration in EBVnGC, and the MiR-BART1-5p inhibitor increases GCNT3 expression, cell proliferation, and migration in transfected GT39 and GT38 cells. NF-kappaB can activate the expression of multiple miR-BARTs, including miR-BART1-5p
additional information
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knockdown of GCNT3 using GCNT3-specific small interfering RNAs: siGCNT3-1 (GCUACUGCGAGCUGUGUAUTT), and siGCNT3-2 (GCUCAGUGCCGUGGAAAUATT). Reduction of the expression of endogenous GCNT3 by siRNA transfection in SGC7901 and BGC823 cells. Epstein-Barr virus (EBV) miRNA miR-BART1-5p specifically targets GCNT3. miR-BART1-5p suppresses GCNT3 expression, cell proliferation, and migration in EBVnGC, and the MiR-BART1-5p inhibitor increases GCNT3 expression, cell proliferation, and migration in transfected GT39 and GT38 cells. NF-kappaB can activate the expression of multiple miR-BARTs, including miR-BART1-5p
additional information
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construction of transgenic mice by microinjection of rat cDNA fused to a rat cardiac-specific promotor into pronuclei of fertilized FVB mouse eggs, overexpression and increase of enzyme activity in the heart leading to cardiac hypertrophy, elevated content of sialylated O-glycans, induction of c-fos expression, and phenotypic changes
additional information
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fusion protein of major histocompatibility complex class II chaperone invariant chain and C2GnT, immunization with this construct leads to reduced growth of Panc02 pancreatic tumor cells
additional information
p48Cre/+-LSL-KrasG12D+þ GEM with Kras mutations display significant dysregulation of EGF receptor and upregulation of mucin biosynthesis in PanIN lesions and pancreatic ductal adenocarcinoma, genotyping
additional information
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p48Cre/+-LSL-KrasG12D+þ GEM with Kras mutations display significant dysregulation of EGF receptor and upregulation of mucin biosynthesis in PanIN lesions and pancreatic ductal adenocarcinoma, genotyping
additional information
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p48Cre/+-LSL-KrasG12D+þ GEM with Kras mutations display significant dysregulation of EGF receptor and upregulation of mucin biosynthesis in PanIN lesions and pancreatic ductal adenocarcinoma, genotyping
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