Information on EC 2.4.1.144 - beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase

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The expected taxonomic range for this enzyme is: Amniota

EC NUMBER
COMMENTARY hide
2.4.1.144
-
RECOMMENDED NAME
GeneOntology No.
beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase
REACTION
REACTION DIAGRAM
COMMENTARY hide
ORGANISM
UNIPROT
LITERATURE
UDP-N-acetyl-D-glucosamine + beta-D-mannosyl-R = UDP + 4-(N-acetyl-beta-D-glucosaminyl)-beta-D-mannosyl-R
show the reaction diagram
REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
hexosyl group transfer
-
-
-
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PATHWAY
BRENDA Link
KEGG Link
MetaCyc Link
mannosyl-glycoprotein N-acetylglucosaminyltransferases
-
-
Metabolic pathways
-
-
N-Glycan biosynthesis
-
-
SYSTEMATIC NAME
IUBMB Comments
UDP-N-acetyl-D-glucosamine:beta-D-mannosyl-glycoprotein 4-beta-N-acetyl-D-glucosaminyltransferase
R represents the remainder of the N-linked oligosaccharide in the glycoprotein acceptor (click here for diagram). The action of this enzyme probably prevents further attachment of N-acetylglucosamine residues to the growing carbohydrate chain.
CAS REGISTRY NUMBER
COMMENTARY hide
83744-93-8
-
ORGANISM
COMMENTARY hide
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
forming normal prion protein PrPC and pathogenic prion protein PrPSc
-
-
Manually annotated by BRENDA team
no activity in Mus musculus
lung melanoma cell line B16-hm
-
-
Manually annotated by BRENDA team
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
malfunction
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knockdown of GnT-III by siRNA causes no alteration in expression levels of E-cadherin mRNA and protein, but induces alterations on E-cadherin cellular localization in MCF-7/AZ cells. GnT-III knockdown cells reveal a membrane de-localization of E-cadherin leading to its cytoplasmic accumulation and cause modifications of E-cadherin N-glycans catalyzed by GnT-III and GnT-V
metabolism
-
N-acetylglucosaminyltransferase-III-mediated glycosylation, specifically on E-cadherin, is a major component of the Epithelial-Mesenchymal-Transition /Mesenchymal-Epithelial-Transition mechanism signature
physiological function
SUBSTRATE
PRODUCT                       
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate) hide
LITERATURE
(Substrate)
COMMENTARY
(Product) hide
LITERATURE
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(beta-D-glucosyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP-D-glucose + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
-
GnT-III catalyzes the removal of the bisecting GlcNAc from the bisected oligosaccharide, producing the corresponding nonbisected sugar chain
-
-
r
UDP-D-glucose + (N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(beta-D-glucosyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
UDP-D-glucose + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(beta-D-glucosyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
-
-
-
-
?
UDP-N-acetyl-D-galactosamine + (N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(N-acetyl-beta-D-galactosaminyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
UDP-N-acetyl-D-glucosamine + (N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-N-acetyl-D-glucosaminyl-2-aminopyridine
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(N-acetyl-beta-D-glucosaminyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-N-acetyl-D-glucosaminyl-2-aminopyridine
show the reaction diagram
-
-
-
ir
UDP-N-acetyl-D-glucosamine + (N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(N-acetyl-beta-D-glucosaminyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
UDP-N-acetyl-D-glucosamine + beta-D-mannosyl-R
UDP + 4-(N-acetyl-beta-D-glucosaminyl)-beta-D-mannosyl-R
show the reaction diagram
-
GnT-III catalyzes the formation of a bisecting GlcNAc structure in N-glycans, resulting in the suppression of metastasis. The priority of GnT-III for the modification of the integrin alpha3 subunit may be an explanation for why GnT-III inhibits GnT-V-induced cell migration. TGnT-III and GnT-V can competitively modify the same target glycoprotein and furthermore positively or negatively regulate its biological functions
-
-
?
UDP-N-acetyl-D-glucosamine + E-cadherin
UDP + E-cadherin with bisecting N-acetyl-D-glucosamine
show the reaction diagram
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recombinant enzyme expressed in murine lung melanoma cells
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-
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UDP-N-acetyl-D-glucosamine + gamma-glutamyltranspeptidase
UDP + gamma-glutamyltranspeptidase with bisecting N-acetyl-D-glucosamine
show the reaction diagram
-
-
?
UDP-N-acetyl-D-glucosamine + GlcNAc-beta-1,2-Man-alpha-1,6-(GlcNAc-beta-1,2-Man-alpha-1,3)-Man-beta-1,4-GlcNAc-beta-1,4-(Fuc-alpha-1,6)-GlcNAc-Asn
UDP + GlcNAc-beta-1,2-Man-alpha-1,6-(GlcNAc-beta-1,2-Man-alpha-1,3)(GlcNAc-beta-1,4)-Man-beta-1,4-GlcNAc-beta-1,4-(Fuc-alpha-1,6)-GlcNAc-Asn
show the reaction diagram
-
-
incorporates a N-acetylglucosamine residue in beta-1,4-linkage to beta-linked mannosyl, i.e. bisecting N-acetylglucosamine, both terminal beta-1,2-linked N-acetylglucosamine residues required for maximum activity, removal of one or both of them reduces activity by 85 or 93%, respectively
ir
UDP-N-acetyl-D-glucosamine + GlcNAc-beta-1,2-Man-alpha-1,6-(GlcNAc-beta-1,2-Man-alpha-1,3)-Man-beta-1,4-GlcNAc-beta-1,4-GlcNAc-2-aminopyridine
UDP + GlcNAc-beta-1,2-Man-alpha-1,6-(GlcNAc-beta-1,2-Man-alpha-1,3)(GlcNAc-beta-1,4)-Man-beta-1,4-GlcNAc-beta-1,4-GlcNAc-2-aminopyridine
show the reaction diagram
-
-
-
-
?
UDP-N-acetyl-D-glucosamine + GlcNAcbeta(1->2)Manalpha(1->6)(GlcNAcbeta(1->2)Manbeta(1->3)Manbeta(1->4)GlcNAcbeta(1->4)GlcNAc-NH(CH2)4NH(2-pyridyl)
?
show the reaction diagram
UDP-N-acetyl-D-glucosamine + transferrin
UDP + transferrin with bisecting N-acetyl-D-glucosamine
show the reaction diagram
-
-
-
?
additional information
?
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NATURAL SUBSTRATES
NATURAL PRODUCTS
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate) hide
LITERATURE
(Substrate)
COMMENTARY
(Product) hide
LITERATURE
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
UDP-N-acetyl-D-glucosamine + (N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(N-acetyl-beta-D-glucosaminyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
show the reaction diagram
UDP-N-acetyl-D-glucosamine + beta-D-mannosyl-R
UDP + 4-(N-acetyl-beta-D-glucosaminyl)-beta-D-mannosyl-R
show the reaction diagram
-
GnT-III catalyzes the formation of a bisecting GlcNAc structure in N-glycans, resulting in the suppression of metastasis. The priority of GnT-III for the modification of the integrin alpha3 subunit may be an explanation for why GnT-III inhibits GnT-V-induced cell migration. TGnT-III and GnT-V can competitively modify the same target glycoprotein and furthermore positively or negatively regulate its biological functions
-
-
?
UDP-N-acetyl-D-glucosamine + E-cadherin
UDP + E-cadherin with bisecting N-acetyl-D-glucosamine
show the reaction diagram
-
recombinant enzyme expressed in murine lung melanoma cells
-
-
-
additional information
?
-
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
INHIBITORS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
ADP-glucose
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competitive against UDP-N-acetyl-D-glucosamine
alpha-N-acetyl-D-glucosamine-1-phosphate
-
-
castanospermine
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activity is not affected, but the enzyme is not localized in the Golgi apparatus
CDP-glucose
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competitive against UDP-N-acetyl-D-glucosamine
EDTA
-
-
GDP-glucose
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competitive against UDP-N-acetyl-D-glucosamine
hepatitis B virus
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selective suppression of enzyme activity on transcription level in transfected cells, e.g. cell line Hb611
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inactive rat mutant D323A enzyme
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acts as an inhibitor of endogenous enzyme activity when expressed in human Huh6 cells
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N-acetyl-D-glucosamine
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TDP-glucose
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competitive against UDP-N-acetyl-D-glucosamine
tunicamycin
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completely abolishes the enzyme activity due to deglycosylation of the enzyme, not localized in the Golgi apparatus
additional information
-
transgenic expression of the enzyme in hepatitis B virus infected cells suppress the virus expression, cell line HB611
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ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
all-trans retinoic acid
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activation
deoxymannojirimycin
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increase in activity, HepG2 and Hep3B cells
forskolin
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induction of the enzyme in hepatoma cells
Triton X-100
tunicamycin
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increase in activity, HepG2 and Hep3B cells
additional information
KM VALUE [mM]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
0.23
(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3)-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R
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-
0.021 - 3.4
pyridylaminated acceptor substrate
1
UDP-D-glucose
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recombinant enzyme
3.6
UDP-N-acetyl-D-galactosamine
-
recombinant enzyme
0.42 - 6.8
UDP-N-acetyl-D-glucosamine
additional information
additional information
-
solid-phase enzyme-linked immunosorbent sandwich assay for enzyme activity
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Ki VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
0.75
ADP-glucose
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recombinant enzyme
3.9
CDP-glucose
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recombinant enzyme
1
GDP-glucose
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recombinant enzyme
SPECIFIC ACTIVITY [µmol/min/mg]
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
0.000000022
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hepatoma cells
0.0000001
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HB611 cells
0.00000013
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normal liver
0.0000004
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HB611 cells treated with interferon-alpha-2a
0.0000009
recombinant enzyme in HeLa cells
0.0000021
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Huh6 cells treated with interferon-alpha-2a
0.0000023
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Huh6 cells
0.0000025
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hepatoma cell line 7721
0.000004
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about, hepatoma cell line 7721, all-trans retinoic acid treated
0.0000096
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fetal primary hepatocytes
0.000012
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purified enzyme
0.0000124
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hepatic carcinoma cells
0.000017
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wild-type and mutant D329A
0.000018
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HepG2 cells
0.000024
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Hep3B cells
0.00006
recombinant enzyme in COS-1 cells
0.000083
-
-
0.02
-
purified recombinant enzyme
5.52
purified enzyme
additional information
-
activity and expression level in various leukemic cells; transcript amount is not correlated to enzyme activity
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
6 - 7
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-
6
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HepG2 cells
6.5
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Hep3B cells
TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
40
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HepG2 cells
43
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Hep3B cells
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
SOURCE
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chronic myelogenous leukemia granulocyte cell lines, e.g. clone KU812 and subclone KU812F
Manually annotated by BRENDA team
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DLD-1/DELTAalpha cells lacking alpha-catenin expression
Manually annotated by BRENDA team
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hepatoblastoma cell line, derived from Huh6 by transfection of 3 copies of hepatitis B virus genome, decreased transcription level
Manually annotated by BRENDA team
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hepatoma cell line
Manually annotated by BRENDA team
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hepatoma cell line
Manually annotated by BRENDA team
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about 100fold increased activity compared to normal liver tissue
Manually annotated by BRENDA team
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hepatoblastoma cell line
Manually annotated by BRENDA team
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multiple myeloma
Manually annotated by BRENDA team
additional information
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY hide
GeneOntology No.
LITERATURE
SOURCE
-
minor fraction
Manually annotated by BRENDA team
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tunicamycin-treated and castanospermine-treated enzyme, not native enzyme
Manually annotated by BRENDA team
MOLECULAR WEIGHT
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
110000
-
about, PAGE
additional information
SUBUNITS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
dimer
-
1 * 63000 + 1 * 53000, SDS-PAGE
POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
glycoprotein
STORAGE STABILITY
ORGANISM
UNIPROT
LITERATURE
-20°C, chicken oviduct microsomal preparation, several months in detergent-free buffer
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Purification/COMMENTARY
ORGANISM
UNIPROT
LITERATURE
; primary structure
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by nickel-chelating affinity chromatography
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primary structure
recombinant His-tagged protein from medium of Spodoptera frugiperda Sf 21 cell culture
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recombinant mutant enzyme from E. coli; wild-type, diethyl(2-hydroxypropyl)aminoethyl-Sepharose and immunoaffinity chromatography
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Cloned/COMMENTARY
ORGANISM
UNIPROT
LITERATURE
; construction of transgenic mice, disruption of certain functions of apolipoprotein B leading to generation of a aftty liver; expression of soluble His-tagged protein in Spodoptera frugiperda Sf 21 insect cells via baculovirus infection, secretion into the medium; expression of wild-type and mutants in COS-1 cells
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amplified for cloning into pENTR-D-Topo vector, cloned gene inserted into the virus expression vector, pBABE-puro. GnT-III and GnT-V constructs transfected into Phoenix-Ampho cells
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cloning from genetic library, DNA sequence determination, functional overexpression in COS-1 or HeLa-cells, transient transfection
cloning of cDNA by RT-PCR
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construction of genes for expression of native rat GnTIII, human ManII, Arabidopsis thaliana ManII and for the expression of the catalytic domains of rat GnTIII and human ManII fused to the N-terminal region of Arabidopsis thaliana ManII. Binary plasmids for high-level expression of rat GnTIII (pAX67), chimeric rat GnTIIIA.th. (replaced native localization domain with the cytoplasmic tail, transmembrane, and stem region of Arabidopsis thaliana mannosidase II) (pAX70), co-expression of rat GnTIII together with human ManII (pAX73) or Arabidopsis thaliana ManII (pAX100), co-expression of GnTIIIA.th. together with ManIIA.th. (pAX74), and co-expression of GnTIIIA.th. and Arabidopsis thaliana ManII (pAX101). Expression of the transgenes is driven by a chimeric promoter assembled from regulatory elements from mannopine and octopine synthase genes. Expression cassettes comprising the CaMV 35S promoter, GnTIII or ManII and the nos pA, being pSK103 (ManII), pSK124 (ManII-Arabidopsis thaliana), pAX63 (GnTIII-Arabidopsis thaliana) and pAX68 (GnTIII) serve as starting point for further expression constructs. The cassette comprising the CaMV 35 promoter, plant relocalized GnTIII and polyadenylation signal is excised from pAX68 using SbfI, EcoRI and inserted into pAX36 generating pAX90. The construct comprising the rat GnTIII obtained by replacing the XbaI, AflII fragment from pAX90 with the fragment isolated from pAX63, generating pAX91. Mutated fragment from pCLF40 inserted into pAX69 using AvaI, StuI, generating pAX104. The binary expression plasmids for inactive GnTIII and GnTIIIA.th. under the control of the UAS123mas promoter generated by replacing the StuI, EcoRI fragment from pAX104 with that in pAX67 (generating pAX105) and pAX70 (generating pAX106), respectively. The mutated fragment from pCLF40 inserted into pAX91 using Eam1105I, StuI, generating the expression plasmid for inactive GnTIII under the control of the CaMV 35S promoter (pAX108). The exchange of the fragment containing the Arabidopsis thaliana Golgi localization domain from pAX90 in pAX108 using SbfI, StuI yields an expression plasmid for inactive GnTIIIA.th. under the control of the CaMV 35S promoter. Plasmids transferred into Agrobacterium tumefaciens LBA4404 for transformation into tobacco BY-2 cells
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construction of transgenic mice, disruption of certain functions of apolipoprotein B leading to generation of a aftty liver; overexpression in rat pheochromocytoma cell line PC-12, glycoproteins contain elevated levels of bisecting GlcNAc, abolished cell differentiation
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expressed in Spodoptera frugiperda Sf21 cells
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expressed in transgenic mice
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expression in erythroleukemia cell line K562, leading to increased resistance to lysis by natural killer cells and enhanced spleen colonization ability; overexpression in murine lung melanoma cell line B16-hm, leading to suppression of the formation of beta-1,6-tri- and tetraantennary N-linked oligosaccharides by inhibiting the responsible enzymes, e.g. N-acetylglucosamine transferase V, EC 2.4.1.155, decrease of the metastatic potential of B16-hm melanoma in vivo, changed phenotype
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expression of a catalytically inactive D232A mutant in human hepatoblastoma cell line Huh6, leading to suppression of the endogenous enzyme activity, but not to a significant decrease in the expression level of the endogenous enzyme; expression of wild-type and mutants in COS-1 cells
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expression of mutant aglycosyl-enzyme, lacking the first 23 amino acid residues, in Escherichia coli
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expression of soluble His-tagged protein in Spodoptera frugiperda Sf 21 insect cells via baculovirus infection, secretion into the medium
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expression of wild-type and mutants in COS-1 cells
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GnT-III overexpressed in MKN45 cells
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GnT-III stable expressing cell lines of Neuro-2a mouse neuroblastoma cells and B16 mouse melanoma cells are established. Overexpression of GnT-III up-regulates adenylyl cyclases activity in Neuro-2a mouse neuroblastoma cells and B16 mouse melanoma cells
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GnT-III transfection into highly pigmented, highly metastatic macrophage-melanoma fusion hybrids results in the suppression of both melanogenesis and motility. The effects of GnT-III appear to occur through inhibition of GnT-V action
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heterozygous alpha 1,3-galactosyltransferase gene knockout pigs produced with transgenic pig fetal cells expressing both human decay-accelerating factor and N-acetylglucosaminyltransferase III
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highly metastatic melanoma B16 cells transfected with GnT-III and then injected into syngeneic mice via the tail vein
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introduction of human N-acetylglucosaminyltransferase gene into tobacco plants leads to highly efficient synthesis of bisected N-glycans. The majority of N-glycans of an antibody produced in a plant expressing GnT-III is also bisected. This might improve the efficacy of therapeutic antibodies produced in this type of transgenic plant; introduction of human N-acetylglucosaminyltransferase (GnT)-III gene into Nicotiana tabacum leads to highly efficient synthesis of bisected N-glycans
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overexpression in HeLa cells, leading to suppression of H2O2-induced activation of PKCdelta-JNK1 signalling pathway resulting in inhibition of apoptosis
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overexpression in murine lung melanoma cell line B16-hm, leading to suppression of the formation of beta-1,6-tri- and tetraantennary N-linked oligosaccharides by inhibiting the responsible enzymes, e.g. N-acetylglucosamine transferase V, EC 2.4.1.155, decrease of the metastatic potential of B16-hm melanoma in vivo, changed phenotype
-
rat GnTIII is expressed either with its native localization domain (GnTIII) or with the cytoplasmic tail, transmembrane domain and stem region (CTS) of Arabidopsis thaliana mannosidase II. N-Glycans of plants expressing rat GnTIII contain three major glycan structures of complex bisected, complex, or hybrid bisected type, accounting for 70%-85% of the total N-glycans. Expression of rat beta(1,4)-N-acetylglucosaminyltransferase III in Nicotiana tabacum remodels the plant-specific N-glycosylation
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Sf21 cells infected with recombinant baculovirus encoding GnT-III
-
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
downregulation of GnT-III expression in MDA-MB-231 cells, an E-cadherin-deficient cell line, the MDCK cell, in which GnTIII expression is undetectable, and fibroblasts, which lack E-cadherin
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during epithelial-mesenchymal-transition, enzyme expression is dramatically decreased and later recoveres when cells return to an epithelial-like phenotype
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E-cadherin-mediated cell-cell interaction upregulates GnT-III expression, suggesting that regulation of GnT-III and E-cadherin expression may exist as a positive feedback loop
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E-cadherin-mediated cell-cell interaction upregulates GnT-III expression. Significant upregulation of GnT-III expression in epithelial cells that express basal levels of E-cadherin and GnT-III
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GnT-III knockdown in MCF-7/AZ cells through siRNA; knockdown of GnT-III, de-localization of E-cadherin and cytoplasmic accumulation, modification of N-glycosylation in E-cadherin
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in MDA-MB231 cells, an E-cadherin-deficient cell line, GnT-III expression is undetectable
-
increase of enzyme expression by wild-type E-cadherin; wild-type E-cadherin regulates MGAT3 gene transcription resulting in increased GnT-III expression. GnT-III mRNA transcription levels in MDA-MB-435 cells transfected with E-cadherin wild-type are ca. 2fold higher than those in MDA-MB-435 mock cells
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shRNA knockdown of beta-catenin results in a dramatic increase in enzyme expression
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significant up-regulation of GnT-III expression in epithelial cells that express basal levels of E-cadherin and GnT-III. Expression levels of GnT-III and its products, the bisected N-glycans, are up-regulated by cell-cell interaction via the E-cadherin-catenin-actin complex. GnT-III expression is significantly up-regulated in cells cultured under dense conditions. Modest increase in GnT-III expression under dense culture conditions in alpha-catenin-deficient DLD-1 cells as well as in E-cadherin-deficient MDA-MB-231 cells. Mutual regulation of GnT-III expression and E-cadherin-mediated cell-cell interaction exists as a positive-feedback loop
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stimulation of the Wnt signaling pathway by the addition of exogenous Wnt3a or SB415286 consistently and significantly inhibits enzyme expression
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the expression levels of GnT-III are suppressed about 25fold in transforming growth factor-beta-treated cells (5 ng/ml)
ENGINEERING
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
D323A
-
expression of a catalytically inactive D232A mutant in human hepatoblastoma cell line Huh6, leading to suppression of the endogenous enzyme activity, but not to a significant decrease in the expression level of the endogenous enzyme; site-directed mutagenesis, expression level in COS-1 cells similar to wild-type, but no remaining catalytic activity
D329A
-
site-directed mutagenesis, unaltered compared to wild-type
N243Q/N261Q
N243Q/N261Q/N399Q
N243Q/N399Q
N261Q/N399Q
APPLICATION
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
medicine
synthesis