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1 n-synthesizing enzyme GCNT3 (core 2 beta-1,6 N-acetylglucosaminyltransferase).
2 cal fringe is also a fucose-specific beta1,3-N-acetylglucosaminyltransferase.
3 hamster ovary cells expressing core2 beta1,6-N-acetylglucosaminyltransferase.
4 which is synthesized by I-branching beta1, 6-N-acetylglucosaminyltransferase.
5 es, which are synthesized by core 2 beta-1,6-N-acetylglucosaminyltransferase.
6 drolyzes UDP-GlcNAc, a sugar donor for Golgi N-acetylglucosaminyltransferases.
7 ein, a proposed substrate of Fringe beta-1,3-N-acetylglucosaminyltransferases.
8 eficient for the glycosyltransferase beta1,3-N-acetylglucosaminyltransferase 1 (beta3GnT1), a key enz
10 cosaminyltransferase (Mgat1), whose product, N-acetylglucosaminyltransferase 1 (GlcNAcT1) is necessar
11 rnatively, protein O-linked mannose beta-1,2-N-acetylglucosaminyltransferase 1 (POMGNT1) catalyzes th
15 ng fukutin, protein O-linked mannose beta1,2-N-acetylglucosaminyltransferase 1 and the fukutin-relate
17 oss of an enzyme (protein O-mannose beta-1,2-N-acetylglucosaminyltransferase 1) that modifies O-manno
18 uding protein O-mannosyltransferase 1, beta3-N-acetylglucosaminyltransferase 1, and like-acetylglucos
20 ed in the Golgi branching pathway, including N-acetylglucosaminyltransferases 1 and 2, which are requ
22 igands elaborated by LSST and core 2 beta1,6-N-acetylglucosaminyltransferase-1 (Core2GlcNAcT) have be
23 -185 targets UDP-N-acetylglucosamine-peptide N-acetylglucosaminyltransferase 110 kDa subunit (OGT1) a
24 by the alternating iterative action of B1,3-N-acetylglucosaminyltransferase 2 (B3GNT2) and B1,4-gala
25 the alternating iterative action of beta1,3-N-acetylglucosaminyltransferase 2 (B3GNT2) and beta1,4-g
29 come-associated genes and found that beta1,6 N-acetylglucosaminyltransferase 2 was downregulated and
33 osyltransferase (C1GalT1) and core 2 beta1,6-N-acetylglucosaminyltransferase-2 or mucus type (C2GnT-M
34 es, beta1,4-galactosyltransferase-I, beta1,3-N-acetylglucosaminyltransferase-2, hCGn6ST, and keratan
35 In this study, we first show that beta1,3-N-acetylglucosaminyltransferase-3 (beta3GlcNAcT-3) is al
37 3 and LNCaP prostate cancer cells with beta3-N-acetylglucosaminyltransferase-6 (core3 synthase) requi
38 LEM domain nuclear lamina component by beta-N-acetylglucosaminyltransferase, a nutrient sensor that
39 an in vitro glycosylation assay to evaluate N-acetylglucosaminyltransferase activity after bacterial
40 d residues that are known to be critical for N-acetylglucosaminyltransferase activity of yeast chitin
41 e proteins possess a fucose-specific beta1,3 N-acetylglucosaminyltransferase activity that initiates
45 ar poly-N-acetyllactosamines, while beta1, 3-N-acetylglucosaminyltransferase and beta4Gal-TI efficien
46 rent cellular proteins catalyzed by O-linked N-acetylglucosaminyltransferase and O-linked N-acetylglu
47 presence of the enzymes for addition (O-beta-N-acetylglucosaminyltransferase) and removal (O-beta-N-a
52 e gene encoding the K. lactis Golgi membrane N-acetylglucosaminyltransferase by complementation of th
53 o the alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase C (MGAT4C) gene on 12q21
55 gulation of the expression of core-2 beta1,6-N-acetylglucosaminyltransferase (C2GnT) 1, a key enzyme
56 nsferase VII (Fuc-T VII) and core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT) are critical for
57 ansgenic mice overexpressing core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT) in T cells, and
58 de is synthesized only when core 2 beta-1, 6-N-acetylglucosaminyltransferase (C2GnT) is present, and
59 ) BW5147 T cells lacking the core 2 beta-1,6-N-acetylglucosaminyltransferase (C2GnT) were resistant t
64 s, we engineered mice lacking core 3 beta1,3-N-acetylglucosaminyltransferase (C3GnT), an enzyme predi
65 and Nod2 agonists upregulated core 3 beta1,3-N-acetylglucosaminyltransferase (C3GnT; an important enz
67 ctions mediated by UDP-GlcNAc:GlcNAc-P-P-Dol N-acetylglucosaminyltransferase (chitobiosyl-P-P-lipid s
68 first demonstrate that I-branching beta1, 6-N-acetylglucosaminyltransferase cloned from human PA-1 e
69 one of the protein subunits of the alpha1-6-N acetylglucosaminyltransferase complex, which catalyses
72 ar cloning of a HEV-expressed core1-beta 1,3-N-acetylglucosaminyltransferase (Core1-beta 3GlcNAcT) en
74 produced glycosyltransferases including key N-acetylglucosaminyltransferases (e.g., GnTI, GnTII, and
76 ne pemphigoid were characterized by marginal N-acetylglucosaminyltransferase expression and decreased
77 the surface of the eye through inhibition of N-acetylglucosaminyltransferase expression in the Golgi.
79 nly non-conserved residue within the beta1,6-N-acetylglucosaminyltransferase family, Cys235, is also
80 ongation of O-fucose on Notch by the beta1,3-N-acetylglucosaminyltransferase Fringe modulates the abi
82 galactosyltransferase or beta1-2- or beta1-6-N-acetylglucosaminyltransferase genes have been found in
83 ynthesized in the presence of core 2 beta1,6-N-acetylglucosaminyltransferase, GlcAT-P, and HNK-1ST.
84 ries glycolipids is catalyzed by the beta1,3 N-acetylglucosaminyltransferase GlcNAc(beta1,3)Gal(beta1
85 s, GlcNAc transfer is mediated by a distinct N-acetylglucosaminyltransferase (GlcNAc-T) activity.
86 of the glycosylating enzyme core 2 beta 1,6-N-acetylglucosaminyltransferase (GlcNAc-T) through prote
87 ty of the regulatory enzyme lactosylceramide N-acetylglucosaminyltransferase (GlcNAc-Tr) with age in
88 lglucosamine (GlcNAc), which is generated by N-acetylglucosaminyltransferase (GnT)-IV, is a good subs
91 nits of the multisubunit enzyme complex, GPI-N-acetylglucosaminyltransferase (GPI-GnT), involved in t
93 (siaA), and the undecaprenyl-phosphate alpha-N-acetylglucosaminyltransferase homolog (wecA) produced
94 significantly lower levels of core 2 beta1,6 N-acetylglucosaminyltransferase I (C2GlcNAcT-I), but no
98 etylglucosamine:alpha-3-D-mannoside beta-1,2-N-acetylglucosaminyltransferase I (GlcNAc-TI, EC 2.4.1.1
99 sulted in a marked and specific reduction in N-acetylglucosaminyltransferase I (GlcNAcT-I) activity a
100 ression of erythropoietin (EPO) in a HEK293S N-acetylglucosaminyltransferase I (GnT I)(-/-) cell line
103 embryonic kidney 293 (HEK293S) cells lacking N-acetylglucosaminyltransferase I (GnTI(-)), and was rec
105 ive alpha-1,2-mannosidase and human beta-1,2-N-acetylglucosaminyltransferase I (GnTI) in the secretor
106 often circumvent this problem by using B1,2-N-acetylglucosaminyltransferase I (MGAT1)-deficient mamm
107 ten circumvent this problem by using beta1,2-N-acetylglucosaminyltransferase I (MGAT1)-deficient mamm
109 , we identified a highly divergent T. brucei N-acetylglucosaminyltransferase I (TbGnTI) among a set o
110 sident UDP-GlcNAc:alpha3-D-mannoside beta1-2-N-acetylglucosaminyltransferase I activity (TbGnTI).
111 the O-glycan branching enzyme core 2 beta1,6-N-acetylglucosaminyltransferase I and its independent re
112 in and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce pa
113 inhibition of glycosylation in the Golgi by N-acetylglucosaminyltransferase I gene inactivation nor
114 his organism, no homologues of the canonical N-acetylglucosaminyltransferase I or II genes can be fou
115 pha-mannosidase I, Nicotiana tabacum beta1,2-N-acetylglucosaminyltransferase I, Arabidopsis Golgi alp
116 y the lowest levels, partial deficiencies in N-acetylglucosaminyltransferase I, II, and V (i.e. Mgat1
117 ialyltransferase, galactosyltransferase, and N-acetylglucosaminyltransferase I, was dramatically disr
118 , the protease was efficiently secreted from N-acetylglucosaminyltransferase I-deficient Lec1 Chinese
119 rate baculovirus, transduce HEK293S GnTI(-) (N-acetylglucosaminyltransferase I-negative) cells in sus
120 ly expressed alpha-2,6-sialyltransferase and N-acetylglucosaminyltransferase-I (NAGT-I), both C-termi
123 ce paucimannosidic N-glycans or elongated by N-acetylglucosaminyltransferase II (GNT-II) to produce c
124 sferase family, encodes an equally divergent N-acetylglucosaminyltransferase II (TbGnTII) activity.
125 insect cell lines lacked adequate endogenous N-acetylglucosaminyltransferase II activity for biantenn
126 ding UDP-GlcNAc:alpha-6-d-mannoside beta-1,2-N-acetylglucosaminyltransferase II enzyme exhibit defici
134 t polylactosamine elongation by knockdown of N-acetylglucosaminyltransferase III or V had no effect o
137 nechocystis sp. strain PCC6803, which encode N-acetylglucosaminyltransferases involved in peptidoglyc
138 tion, suggesting developmental regulation of N-acetylglucosaminyltransferases IV and V and alpha6-fuc
139 thermore, the mRNA and protein expression of N-acetylglucosaminyltransferase IVa (GnT-IVa), which was
140 of this capsular polysaccharide involves in N-acetylglucosaminyltransferase (KfiA) and d-glucuronylt
142 g), which encodes an O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase known to modify epiderma
143 e 2 branching enzyme, termed core 2 beta-1,6-N-acetylglucosaminyltransferase-leukocyte type (C2GnT-L)
145 ession of reporter N-linked glycoproteins in N-acetylglucosaminyltransferase MGAT1-null HEK293 cells
147 is (hexosamine pathway) and in turn to Golgi N-acetylglucosaminyltransferases Mgat1, -2, -4, and -5.
148 that alpha-1,3-Mannosyl-Glycoprotein 2-beta-N-Acetylglucosaminyltransferase (MGAT1) served as the pi
149 mannosyl (alpha-1,3-)-glycoprotein beta-1,2-N-acetylglucosaminyltransferase (MGAT1), necessary for t
150 enes (alpha-1,3-mannosyl-glycoprotein 2-beta-N-acetylglucosaminyltransferase (MGAT1), transducing-lik
151 mannosyl (alpha-1,3-)-glycoprotein beta-1,2- N-acetylglucosaminyltransferase (Mgat1), whose product,
152 ion of beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase (MGAT3) (P < 0.001) and
153 mannosyl (alpha-1,3-)-glycoprotein beta-1,4-N-acetylglucosaminyltransferase (Mgat4) with UDP-GlcNAc.
154 mannosyl (alpha-1,6-)-glycoprotein beta-1,6-N-acetylglucosaminyltransferase (Mgat5) in the Golgi mem
157 ogue of the cellular core 2 protein beta-1,6-N-acetylglucosaminyltransferase-mucin type (C2GnT-M), wh
158 fication of a thermostable archaeal beta-1,4-N-acetylglucosaminyltransferase, named archaeal glycosyl
160 c mutation in the gene encoding the alpha1-6-N-acetylglucosaminyltransferase necessary for the format
161 ligosaccharides on the physiology of plants, N-ACETYLGLUCOSAMINYLTRANSFERASE (NodC) of Azorhizobium c
162 ering the expression or activity of O-linked N-acetylglucosaminyltransferase, O-linked N-acetylglucos
163 r GnT1IP-L inhibits other N-glycan branching N-acetylglucosaminyltransferases of the medial Golgi.
165 her, the mRNA for nucleocytoplasmic O-linked N-acetylglucosaminyltransferase (OGT) increases 3.4-fold
166 tter did not have a soluble inhibitor of the N-acetylglucosaminyltransferase or a hexosaminidase that
167 n ligand-synthesizing enzymes core-2 beta1,6-N-acetylglucosaminyltransferase or fucosyltransferases I
168 ion is evident in protein O-mannose beta-1,2-N-acetylglucosaminyltransferase (POMGnT1) knockout mouse
170 have identified an enzyme, polypeptide alpha-N-acetylglucosaminyltransferase (pp alpha-GlcNAc-T2), th
171 mZP3 and huZP3 affect the ability of core 2 N-acetylglucosaminyltransferase(s) to extend the core 1
172 the B3GNT7 transcript, which encodes a B1-3-N-acetylglucosaminyltransferase that can participate in
173 e B3GNT7 transcript, which encodes a beta1-3-N-acetylglucosaminyltransferase that can participate in
174 pressed in cultured cells inhibit MGAT1, the N-acetylglucosaminyltransferase that initiates the synth
176 -fucosyltransferase-1) and Fringe, a beta1,3-N-acetylglucosaminyltransferase that modifies O-fucose i
178 inge proteins are O-fucose-specific beta-1,3 N-acetylglucosaminyltransferases that glycosylate the ex
179 nd Radical Fringe (LFNG, MFNG, and RFNG) are N-acetylglucosaminyltransferases that modify Notch recep
182 ent in milk and the recently cloned beta-1,3-N-acetylglucosaminyltransferase, the formation of poly-N
183 xture of beta4Gal-TI and i-extension beta1,3-N-acetylglucosaminyltransferase, the major product was t
189 small interfering RNA-directed knockdown of N-acetylglucosaminyltransferase V (GnT-V), a glycosyltra
190 human clinical samples, we demonstrated that N-acetylglucosaminyltransferase V (GnT-V)-mediated glyco
194 s, including branched N-glycans generated by N-acetylglucosaminyltransferase V (Mgat5) activity, form
195 chanistically, ALK4 loss upregulates beta1,6 N-acetylglucosaminyltransferase V (MGAT5) and galectin-3
197 ed that beta1,6GlcNAc-branched complex-type (N-acetylglucosaminyltransferase V (Mgat5)) N-glycans on
198 cetylglucosamine:alpha-6-D-mannoside beta1,6-N-acetylglucosaminyltransferase V (MGAT5)-modified N-gly
199 Lec4 and Lec13 cells, which are defective in N-acetylglucosaminyltransferase V and GDP-fucose synthes
200 h aberrant N-glycosylation caused by altered N-acetylglucosaminyltransferase V(GnT-V, GnT-Va, and Mga
201 experiments indicated that HG-CD147 contains N-acetylglucosaminyltransferase V-catalyzed, beta1,6-bra
202 A glycosyltransferase that branches O-Man, N-acetylglucosaminyltransferase Vb (GnT-Vb), is highly e
203 hether Fringe, an O-fucose specific beta 1,3-N-acetylglucosaminyltransferase, was capable of modifyin
204 reover, beta4Gal-TIV, together with beta-1,3-N-acetylglucosaminyltransferase, was capable of synthesi
205 e identified one glycosyltransferase, core 2 N-acetylglucosaminyltransferase, which is down-regulated
206 TDC2) is a protein O-linked mannose beta 1,4-N-acetylglucosaminyltransferase whose product could be e
207 Here we report this enzyme is not a beta-1,3-N-acetylglucosaminyltransferase with catalytic activity