Any feedback?
Information on EC 2.4.1.122 - N-acetylgalactosaminide beta-1,3-galactosyltransferase and Organism(s) Homo sapiens and UniProt Accession O75752
for references in articles please use BRENDA:EC2.4.1.122Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
EC Tree
2.4.1.122 N-acetylgalactosaminide beta-1,3-galactosyltransferaseIUBMB Comments
The eukaryotic enzyme can act on non-reducing O-serine-linked N-acetylgalactosamine residues in mucin glycoproteins, forming the T-antigen. The bacterial enzyme, found in some pathogenic strains, is involved in biosynthesis of the O-antigen repeating unit.
Specify your search results
Word Map
- 2.4.1.122
-
galactosylation
- glycosyltransferases
- oligosaccharide
- n-acetylglucosamine
- apparatus
- milk
-
sialyltransferase
- alpha-lactalbumin
- glcnac
- o-glycans
- lectin
- epitope
-
o-glycosylation
- glycolipids
-
o-linked
-
sialylated
-
sialic
-
fucosyltransferase
- ganglioside
- glycoconjugates
- glycopeptides
- agglutinin
-
trans-golgi
-
n-acetylglucosaminyltransferase
-
cisterna
- 5'-nucleotidase
-
xenotransplantation
- lactosylceramide
-
n-acetylgalactosaminyltransferase
- n-acetyllactosamine
- iga1
- glycosphingolipids
-
fucosylated
-
hyperacute
-
alpha1,3
- gm2
-
3hgalactose
- trisaccharide
-
submaxillary
- glucosylceramide
-
anti-gal
- pellucida
-
cmp-sialic
- ovomucoid
- galactans
-
xenoantigens
-
mannosyltransferase
-
1-4glcnac
-
golgi-enriched
-
xylosyltransferase
- medicine
- diagnostics
The taxonomic range for the selected organisms is: Homo sapiens
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria
Reaction Schemes
Synonyms
galactosyltransferase, c1galt1, t-synthase, beta-galactosyltransferase, c1galt, core 1 synthase, dc1galt1, core 1 beta3-gal-t, ce-t-synthase, core 1 beta3-gal-transferase, 
more
topSYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
C1GalT
C1GALT1
core 1 beta1,3-galactosyltransferase
galactosyltransferase, uridine diphosphogalactose-mucin beta-(1-3)-
-
-
-
-
uridine diphosphogalactose-mucin beta-(1-3)-galactosyltransferase
-
-
-
-
REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
hexosyl group transfer
-
-
-
-
PATHWAY SOURCE
PATHWAYS
BRENDA
-
-, -, -, -
SYSTEMATIC NAME
IUBMB Comments
UDP-alpha-D-galactose:N-acetyl-alpha-D-galactosaminyl-R beta-1,3-galactosyltransferase (configuration-inverting)
The eukaryotic enzyme can act on non-reducing O-serine-linked N-acetylgalactosamine residues in mucin glycoproteins, forming the T-antigen. The bacterial enzyme, found in some pathogenic strains, is involved in biosynthesis of the O-antigen repeating unit.
CAS REGISTRY NUMBER
COMMENTARY
97089-61-7
-
SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
UDP-galactose + ganglioside Gg3
UDP + galactosyl-beta-1,3-ganglioside Gg3
i.e. GalNAcbeta1,4-Galbeta1,4-Glcbeta1-ceramide
-
?
UDP-galactose + ganglioside GM2
UDP + galactosyl-beta-1,3-ganglioside GM2
i.e. GalNAcbeta1,4-(NeuAcalpha-2,3-)Galbeta1,4-Glcbeta1-ceramide
i.e. ganglioside GM1
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
UDP-galactose + Ac-GHA-(GalNAcalpha1-)TSLPVTG-NH2
UDP + Ac-GHA-(Galbeta1-3GalNAcalpha1-)TSLPVTG-NH2
pH 7.0, 0.2 mM, 750% activity in H292-cells, 550% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + Ac-SCSTGHA-(GalNAcalpha1-)TSG-NH2
UDP + Ac-SCSTGHA-(Galbeta-1-3GalNAcalpha1-)TSG-NH2
pH 7.0, 0.2 mM, 50% activity in H292-cells, 40% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + Ac-STGHA-(GalNAcalpha1-)TSLPG-NH2
UDP + Ac-STGHA-(Galbeta1-3GalNAcalpha1-)TSLPG-NH2
pH 7.0, 0.2 mM, 425% activity in H292-cells, 275% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + Ac-SVS-(GalNAcalpha1-)TGHATSG-NH2
UDP + Ac-SVS-(Galbeta1-3GalNAcalpha1-)TGHATSG-NH2
pH 7.0, 0.2 mM, 300% activity in H292-cells, 450% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + Ac-TSSVS-(GalNAcalpha1-)TGHAG-NH2
UDP + Ac-TSSVS-(Galbeta1-3GalNAcalpha1-)TGHAG-NH2
pH 7.0, 0.2 mM, 400% activity in H292-cells, 4000% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + asialo ovine submaxillary mucin
UDP + beta-D-galactosyl-1,3-N-acetylgalactosyl-asialo ovine submaxillary mucin
-
-
-
?
UDP-galactose + asialo-agalacto-glycophorin
UDP + beta-D-galactosyl-1,3-N-acetylgalactosyl-asialo-agalacto-glycophorin
-
-
-
?
UDP-galactose + benzyl 2-(acetylamino)-2-deoxy-alpha-D-galactopyranoside
UDP + benzyl 2-(acetylamino)-2-deoxy-3-O-beta-D-galactopyranosyl-alpha-D-galactopyranoside
pH 7.0, 2 mM, 100% activity in H292-cells, 100% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-(1->3)-N-acetyl-D-galactosamine
-
-
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
UDP-galactose + N-acetyl-alpha-D-galactosaminyl-phenyl
UDP + beta-D-galactosyl-1,3-N-acetyl-alpha-D-galactosaminyl-phenyl
-
-
?
UDP-galactose + N-acetylgalactosaminide mucin
UDP + beta-D-galactosyl-1,3-N-acetylgalactosaminide mucin
-
-
-
-
?
UDP-galactose + p-nitrophenyl-beta-N-acetylgalactosamide
UDP + beta-D-galactosyl-1,3-N-acetylgalactosyl-p-nitrophenyl
-
-
-
?
UDP-galactose + TTTV-(GalNAcalpha1-)TPTPTG
UDP + TTTV-(Galbeta1-3GalNAcalpha1-)TPTPTG
pH 7.0, 0.2 mM, 50% activity in H292-cells, 90% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + TTTVTP-(GalNAcalpha1-)TPTG
UDP + TTTVTP-(Galbeta1-3GalNAcalpha1-)TPTG
pH 7.0, 0.2 mM, 110% activity in H292-cells, 60% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + TTTVTPTP-(GalNAcalpha1-)TG
UDP + TTTVTPTP-(Galbeta1-3GalNAcalpha1-)TG
pH 7.0, 0.2 mM, 65% activity in H292-cells, 60% activity in A549 cells relative to 1-O-benzyl-N-acetyl-D-galactosamine
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
-
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
-
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
-
i.e. core 1 structure
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
threonine alpha-D-galactosamine is preferred to serine alpha-D-galactosamine
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
high specificity for N-acetylgalactosaminyl residues linked to serine or threonine
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
enzyme is important in O-glycan biosynthesis in digestive organs
-
-
?
additional information
?
-
-
no acceptor substrates: ovalbumin, beta-N-acetyl-D-glucosaminyl-benzyl
-
-
?
additional information
?
-
no acceptor substrates: ovalbumin, beta-N-acetyl-D-glucosaminyl-benzyl
-
-
?
additional information
?
-
-
elevated preferences for Gly at the +1 position with moderately high preferences for Phe and Tyr in the +3 position relative to the acceptor Thr-O-GalNAc
-
-
?
additional information
?
-
-
core 1 synthase specific molecular chaperone is essential for the expression of functional enzyme
-
-
?
NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-(1->3)-N-acetyl-D-galactosamine
-
-
-
-
?
UDP-galactose + glycoprotein N-acetyl-D-galactosamine
UDP + glycoprotein D-galactosyl-1,3-N-acetyl-D-galactosamine
enzyme is important in O-glycan biosynthesis in digestive organs
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
-
-
?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
-
-
-
?
additional information
?
-
-
elevated preferences for Gly at the +1 position with moderately high preferences for Phe and Tyr in the +3 position relative to the acceptor Thr-O-GalNAc
-
-
?
additional information
?
-
-
core 1 synthase specific molecular chaperone is essential for the expression of functional enzyme
-
-
?
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
itraconazole
itraconazole is a C1GALT1 inhibitor that directly binds C1GALT1 and promotes its proteasomal degradation, leading to significant blockade of C1GALT1-mediated effects in HNSCC cells in vitro and in vivo
itraconazole
mediates its suppressive effects on malignant phenotypes and EGFR activity by inhibiting C1GALT1 in HNSCC cells. C1GALT1 inhibitor itraconazole can also suppress tumor growth
additional information
homology modeling and docking simulation with potential C1GALT1 inhibitors
-
additional information
-
homology modeling and docking simulation with potential C1GALT1 inhibitors
-
ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
lactacystin
-
treatment with 0.01 mM lactacystin results in the increased expression of C1GalT protein
SPECIFIC ACTIVITY [µmol/min/mg]
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
additional information
additional information
-
inactive HPC4-tagged soluble T-synthase regained activity within 5 min after the addition of chaprone 6His-sCosmc, at 37°C
additional information
-
T-synthase may utilize charge-charge interactions to modulate its activity, rejecting basic peptides over neutral and acidic peptide acceptors, T-synthase recognizes specific features of the peptide portion of the substrate, including overall charge and the presence of Gly, Phe, Tyr, and perhaps Pro at specific positions, up to four residues from the site of glycosylation, and indeed may use these features to modulate sites of Core 1 glycosylation
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
pH RANGE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
37
ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
additional information
C1GALT1 expression is upregulated in HNSCC tumors
-
C1GALT1 expression is upregulated in HNSCC tumors
additional information
-
no endogenous activity in Jurkat and LSC, a colorectal cell line, cells
additional information
no endogenous activity in Jurkat and LSC, a colorectal cell line, cells
additional information
no endogenous activity in Jurkat and LSC, a colorectal cell line, cells
additional information
C1GALT1 is overexpressed in various human malignancies
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
additional information
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
malfunction
physiological function
additional information
malfunction
-
mutations in the chaperone Cosmc, which is encoded by the X-chromosome gene (Xq24) in humans, leads to loss of T-synthase activity and expression of the abnormal Tn (GalNAc1-Ser/Thr) and Sialyl Tn (NeuAc2-3GalNAc1-Ser/Thr) antigens, which are also known as tumor-associated carbohydrate antigens, Tn syndrome is a rare autoimmune disease in which subpopulations of blood cells in all lineages carry an incompletely glycosylated membrane
malfunction
-
abrogation of the enzyme promotes membrane protein internalization. Disruption of core 1 O-glycosyltransferase activity induces endocytosis and faster accumulation of cell surface proteins in cytoplasmic vesicles and induces clathrin-mediated endocytosis. Enzyme-deficient human corneal keratinocytes display plasma membrane invaginations on the apical surface
malfunction
C1GALT1 overexpression enhances HNSCC cell viability, migration, and invasion, which can be reversed by erlotinib. Silencing of C1GALT1 suppresses the malignant behavior both in vitro and in vivo. C1GALT1 knockdown decreases the EGFR signaling in SAS, OEC-M1, and FaDu cells. Decreased C1GALT1 causes accumulation of Tn antigens
malfunction
core 1 beta1,3-galactosyltransferase (C1GALT1) expression is upregulated in HNSCC tumors and is associated with adverse clinicopathologic features. Moreover, high C1GALT1 expression predicts poor disease-free and overall survivals. C1GALT1 overexpression enhances HNSCC cell viability, migration, and invasion, which can be reversed by erlotinib. Silencing of C1GALT1 suppresses the malignant behavior both in vitro and in vivo. Blocking O-glycan elongation on epidermal growth factor receptor (EGFR) by C1GALT1 knockdown decreases EGF-EGFR binding affinity and inhibits EGFR signaling, thereby suppressing malignant phenotypes. C1GALT1 knockout also decreases the EGFR signaling in SAS cells as shown in two independent clones. C1GALT1 overexpression in SAS cells increases EGF-induced phosphorylation of EGFR at Y1068. By contrast, C1GALT1 knockdown decreases the EGFR signaling in OEC-M1 and FaDu cells. Decreased C1GALT1 causes accumulation of Tn antigens, which is detected by vicia villosa agglutinin (VVA) lectin
physiological function
-
T-synthase is the key beta3-galactosyltransferase essential for biosynthesis of core 1 O-glycans (Gal beta1-3GalNAc alpha1-Ser/Thr) in animal cell glycoproteins
physiological function
-
core 1 O-glycosylation is required to maintain transcellular barrier function. Core 1 O-glycans contribute to maintenance of apical barrier function on exposed mucosal surfaces by preventing clathrin-mediated endocytosis
physiological function
core 1 beta1,3-galactosyltransferase (C1GALT1) controls the crucial step of GalNAc-type O-glycosylation and is overexpressed in various human malignancies with a role in head and neck squamous cell carcinoma (HNSCC). Enzyme C1GALT1 seems to promote in vitro disease progression in ovarian cancer. C1GALT1 modifies O-glycans on epidermal growth factor receptor (EGFR). C1GALT1 regulates phosphorylation, EGF-binding affinity, and O-glycosylation of EGFR to enhance malignant phenotypes in HNSCC cells. C1GALT1 regulates EGF-binding affinity of EGFR in HNSCC cells. C1GALT1 transfers galactose to Tn antigen to form T antigen. C1GALT1 is overexpressed in head and neck squamous cell carcinoma (HNSCC) tumors and high C1GALT1 expression predicts poor prognosis
physiological function
core 1 beta1,3-galactosyltransferase (C1GALT1) controls the crucial step of GalNAc-type O-glycosylation. C1GALT1 regulates phosphorylation, EGF-binding affinity, and O-glycosylation of EGFR to enhance malignant phenotypes in HNSCC cells. Itraconazole blocks C1GALT1-mediated malignant phenotypes and EGFR activity, overview. C1GALT1 transfers galactose to Tn antigen to form T antigen
additional information
C1GALT1 is overexpressed in various human malignancies
UNIPROT
ENTRY NAME
ORGANISM
NO. OF AA
NO. OF TRANSM. HELICES
MOLECULAR WEIGHT[Da]
SOURCE
SEQUENCE
LOCALIZATION PREDICTION
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable).
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable). MOLECULAR WEIGHT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SUBUNIT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
additional information
additional information
itraconazole is a C1GALT1 inhibitor that directly binds C1GALT1 and promotes its proteasomal degradation, leading to significant blockade of C1GALT1-mediated effects in HNSCC cells in vitro and in vivo
additional information
-
itraconazole is a C1GALT1 inhibitor that directly binds C1GALT1 and promotes its proteasomal degradation, leading to significant blockade of C1GALT1-mediated effects in HNSCC cells in vitro and in vivo
additional information
the effect of itraconazole on C1GALT1 protein levels might be through posttranslational modifications, analysis of mechanism by which itraconazole promotes C1GALT1 degradation
additional information
-
the effect of itraconazole on C1GALT1 protein levels might be through posttranslational modifications, analysis of mechanism by which itraconazole promotes C1GALT1 degradation
PURIFICATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
functional expression in Spodoptera frugiperda Sf9cells via baculovirus infection
DNA and amino acid sequence determination and analysis, transient functional expression in human 293T cells as wild-type and soluble, i.e. secreted into the medium, epitope-tagged protein, stable functional expression of the soluble epitope-tagged enzyme in CHO-K1 and Lec1-CHO cells
DNA sequence determination, functional expression in human LSC cells
soluble T-synthase is made by co-expressing N-terminal HPC4 epitope-tagged soluble T-synthase with wild-type full-length Cosmc in Hi-5 insect cells using the Baculovirus system
-
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
real-time RT-PCR analysis shows that C1GALT1 messenger RNA expression is not significantly affected, implying that the effect of itraconazole on C1GALT1 protein levels might be through posttranslational modifications. Itraconazole increases ubiquitinated C1GALT1. C1GALT1 degradation induced by itraconazole is primarily through the proteasomal degradation pathway
RENATURED/Commentary
ORGANISM
UNIPROT
LITERATURE
the chaperone Cosmc promotes renaturation of denatured T-synthase in vitro, HPC4-tagged soluble T-synthase is denatured in 1 ml of 6 M guanidinium hydrochloride, pH 7.2 for 90 min at room temperature, the sample is diluted 100times in reconstitution buffer (10 mM HEPES, 150 mM NaCl, 12 mM MgCl2, pH 7.8), reconstitution is initiated by the addition of 6His-sCosmc and ATP where the final concentration is 2.27 microM and 5 mM, reaction is incubated for 45 min at room temperature, 6His-sCosmc can cause up to 75% restoration of heat-denatured HPC4-tagged soluble T-synthase activity depending on how long the protein is heat-treated, and that it can restore 30% of activity to HPC4-tagged soluble T-synthase denatured by guanidinium hydrochloride treatment
-
APPLICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
diagnostics
C1GALT1 predicts poor prognosis and is a potential therapeutic target in head and neck cancer
medicine
medicine
-
polymorphisms of the C1GALT1 gene are associated with the genetic susceptibility to IgA nephropathy in Chinese population
medicine
C1GALT1 predicts poor prognosis and is a potential therapeutic target in head and neck cancer
REF.
AUTHORS
TITLE
JOURNAL
VOL.
PAGES
YEAR
ORGANISM (UNIPROT)
PUBMED ID
SOURCE
Amado, M.; Almeida, R.; Carneiro, F.; Levery, S.B.; Holmes, E.H.; Nomoto, M.; Hollingsworth, M.A.; Hassan, H.; Schwientek, T.; Nielsen, P.A.; Bennett, E.P.; Clausen, H.
A family of human beta3-galactosyltransferases. Characterization of four members of a UDP-galactose:beta-N-acetyl-glucosamine/beta-acetyl-galactosamine beta-1,3-galactosyltransferase family
J. Biol. Chem.
273
12770-12778
1998
Homo sapiens, Homo sapiens (O75752)
Hesford, F.J.; Berger, E.G.; Van den Eijnden, D.H.
Identification of the product formed by human erythrocyte galactosyltransferase
Biochim. Biophys. Acta
659
302-311
1981
Homo sapiens
Ju, T.; Brewer, K.; D'Souza, A.; Cummings, R.D.; Canfield, W.M.
Cloning and expression of human core 1 beta1,3-galactosyltransferase
J. Biol. Chem.
277
178-186
2002
Caenorhabditis elegans (Q18515), Caenorhabditis elegans, Rattus norvegicus (Q9JJ05), Mus musculus (Q9JJ06), Mus musculus, Homo sapiens (Q9NS00), Homo sapiens
Kudo, T.; Iwai, T.; Kubota, T.; Iwasaki, H.; Takayma, Y.; Hiruma, T.; Inaba, N.; Zhang, Y.; Gotoh, M.; Togayachi, A.; Narimatsu, H.
Molecular cloning and characterization of a novel UDP-Gal:GalNAcalpha peptide beta1,3-galactosyltransferase (C1Gal-T2), an enzyme synthesizing a core 1 structure of O-glycan
J. Biol. Chem.
277
47724-47731
2002
Homo sapiens, Homo sapiens (Q96EU7), Homo sapiens (Q9NS00)
Narimatsu, Y.; Ikehara, Y.; Iwasaki, H.; Nonomura, C.; Sato, T.; Nakanishi, H.; Narimatsu, H.
Immunocytochemical analysis for intracellular dynamics of C1GalT associated with molecular chaperone, Cosmc
Biochem. Biophys. Res. Commun.
366
199-205
2008
Homo sapiens
Li, G.S.; Zhang, H.; Lv, J.C.; Shen, Y.; Wang, H.Y.
Variants of C1GALT1 gene are associated with the genetic susceptibility to IgA nephropathy
Kidney Int.
71
448-453
2007
Homo sapiens
Buck, K.S.; Smith, A.C.; Molyneux, K.; El-Barbary, H.; Feehally, J.; Barratt, J.
B-cell O-galactosyltransferase activity, and expression of O-glycosylation genes in bone marrow in IgA nephropathy
Kidney Int.
73
1128-1136
2008
Homo sapiens
Brockhausen, I.; Dowler, T.; Paulsen, H.
Site directed processing: role of amino acid sequences and glycosylation of acceptor glycopeptides in the assembly of extended mucin type O-glycan core 2
Biochim. Biophys. Acta
1790
1244-1257
2009
Homo sapiens (Q9NS00)
Perrine, C.; Ju, T.; Cummings, R.D.; Gerken, T.A.
Systematic determination of the peptide acceptor preferences for the human UDP-Gal:glycoprotein-alpha-GalNAc beta 3 galactosyltransferase (T-synthase)
Glycobiology
19
321-328
2009
Homo sapiens
Aryal, R.P.; Ju, T.; Cummings, R.D.
The endoplasmic reticulum chaperone Cosmc directly promotes in vitro folding of T-synthase
J. Biol. Chem.
285
2456-2462
2010
Homo sapiens
Narimatsu, Y.; Kubota, T.; Furukawa, S.; Shimojima, M.; Iwasaki, H.; Tozawa, Y.; Tachibana, K.; Narimatsu, H.
Co-translational function of Cosmc, core 1 synthase specific molecular chaperone, revealed by a cell-free translation system
FEBS Lett.
585
1276-1280
2011
Homo sapiens
Guzman-Aranguez, A.; Woodward, A.M.; Pintor, J.; Argueeso, P.
Targeted disruption of core 1 beta1,3-galactosyltransferase (C1galt1) induces apical endocytic trafficking in human corneal keratinocytes
PLoS ONE
7
e36628
2012
Homo sapiens
Chou, C.H.; Huang, M.J.; Liao, Y.Y.; Chen, C.H.; Huang, M.C.
C1GALT1 seems to promote in vitro disease progression in ovarian cancer
Int. J. Gynecol. Cancer
27
863-871
2017
Homo sapiens (Q9NS00), Homo sapiens
EXTERNAL LINKS (specific for EC-Number 2.4.1.122)
Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.
Release 2023.1 (January 2023)
Legal
Curated at
Member of
