2.4.1.150: N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase
This is an abbreviated version!
For detailed information about N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase, go to the full flat file.
Word Map on EC 2.4.1.150
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2.4.1.150
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cataract
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poly-n-acetyllactosamine
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cryaa
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n-acetyllactosamine
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polylactosamines
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glycan-binding
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diagnostics
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pharmacology
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medicine
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synthesis
- 2.4.1.150
- cataract
- poly-n-acetyllactosamine
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cryaa
- n-acetyllactosamine
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polylactosamines
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glycan-binding
- diagnostics
- pharmacology
- medicine
- synthesis
Reaction
Synonyms
2beta-1,6-acetylglucosaminyltransferase, acetylglucosaminyltransferase, uridine diphosphoacetylglucosamine-acetyllactosaminide beta1-->6-, beta1-6GnT, C2/4GnT, C24GNT, C2GnT, C2GnT2, C2GNTM, core 2 beta-1,6-N-acetylglucosaminyltransferase, core 2beta-1,6-acetylglucosaminyltransferase, dIHnT, distally acting I-branching beta1,6-N-acetylglucosaminyltransferase, EC 2.4.1.164, Galbeta1-->4GlcNAc-R beta1-->6 N-acetylglucosaminyltransferase, GCNT2, Gcnt2 gene product, gcnt3, glucosaminyl (N-acetyl) transferase 2, GNTM, I beta1,6-N-acetylglucosaminyltransferase, I N-acetylglucosaminyltransferase, I-branching beta-1,6-N-acetylglucosaminyl transferase 2, I-branching beta-1,6-N-acetylglucosaminyltransferase, I-branching enzyme, I-branching N-acetylglucosaminyltransferase, IGnT, More, N-acetylglucosaminyltransferase, N-acetyllactosaminide beta-1,6-N-acetylglucosaminyl-transferase, UDP-GlcNAc:Gal-R, beta-D-6-N-acetylglucosaminyltransferase, UDP-N-acetyl-D-glucosamine:beta-D-galactosyl-(1->4)-N-acetyl-D-glucosaminide 6-beta-N-acetyl-D-glucosaminyltransferase, uridine diphosphoacetylglucosamine-acetyllactosaminide beta1-->6-acetylglucosaminyltransferase
ECTree
2.4.1.150 N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferaseAdvanced search results
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Engineering on EC 2.4.1.150 - N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
A169T
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
G310D
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
G334R
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
G348E
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
N388R
homozygous frameshift mutation c.1163_1166delATCA, p.(Asn388Argfs*20) is the cause of congenital cataract in two affected siblings, pleiotropic effect of the mutation causing congenital cataract and adult I blood group phenotype, overview
R226Q
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
R383H
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
W326stop
naturally occuring mutation in the GCNT2 gene causing blood group I and cataract formation phenotype
additional information
additional information
CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells
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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mutation experiments at the GT boxes of the promoters of IGnT A and B genes
additional information
CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells. A significant increase in pancreas weight is observed in Kras mice compared with wild-type mice. Only 6% of the pancreata from Kras mice are free from PanIN lesions and PDAC, whereas 100% of pancreata are normal in wild-type mice
additional information
Mus musculus C5BL/6
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CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells. A significant increase in pancreas weight is observed in Kras mice compared with wild-type mice. Only 6% of the pancreata from Kras mice are free from PanIN lesions and PDAC, whereas 100% of pancreata are normal in wild-type mice
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