ライフサイエンスコーパス: GlcNAc

1 GlcNAc can be added to proteins by O-GlcNAc transferase

2 (COSMC), N-glycans by targeting the beta1,2 GlcNAc-transferase (MGAT1) and GSLs by deleting UDP-gluc

3 array demonstrated GalNAcbeta1-4(Fucalpha1-3)GlcNAc (LDNF) as a specific Y3-binding ligand.

4 n B because of the presence of Galbeta(1-->4)GlcNAc ligands on chicken ovalbumin.

5 samine (LacNAc), and unnatural Galalpha(1,4)-GlcNAc and Manbeta(1,4)-GlcNAc appendages.

6 atural Galalpha(1,4)-GlcNAc and Manbeta(1,4)-GlcNAc appendages.

7 te that is selectively modified with beta1,6 GlcNAc-branched N-glycans catalyzed by GnT-V.

8 omain with a cavity that could accommodate a GlcNAc moiety.

9 Thus, fungi use Ngs1 as a GlcNAc-sensor and transducer for GlcNAc-induced transcri

10 ino acid, peptide or protein that contains a GlcNAc residue as an acceptor.

11 responsible for the sequential addition of a GlcNAc and two rhamnoses, respectively, and that GT3 is

12 ed enzyme concluded that the attachment of a GlcNAc on the alpha1,3 mannose arm of N-glycan is essent

13 Charcot-Marie-Tooth neuropathy, has abundant GlcNAc-6-O-sulfated N-glycans.

14 soenzymes that transfer N-acetylglucosamine (GlcNAc) and glucuronic acid (GlcUA) in alternative posit

15 ractions, with glucose, N-acetylglucosamine (GlcNAc) and mannose in between.

16 smic proteins with beta-N-acetylglucosamine (GlcNAc) and regulates numerous biological processes.

17 leting two Bdellovibrio N-acetylglucosamine (GlcNAc) deacetylases, one of which we show to have a uni

18 N-acetylglucosamine (GlcNAc) exists ubiquitously as a component of the surfac

19 ties for derivatives of N-acetylglucosamine (GlcNAc) in aqueous solution.

20 -translational O-linked N-acetylglucosamine (GlcNAc) modification.

21 requires alpha- or beta-N-acetylglucosamine (GlcNAc) moieties on cell wall teichoic acid (WTA) for ad

22 he O-linked addition of N-acetylglucosamine (GlcNAc) moieties to Ser and Thr residues.

23 tached to the remaining N-acetylglucosamine (GlcNAc) of IgG, using a mutant endoglycosidase (also cal

24 trates which contain an N-acetylglucosamine (GlcNAc) residue to act as an 'acceptor' handle.

25 e of CPS and the beta-D-N-acetylglucosamine (GlcNAc) residues of peptidoglycan (PG).

26 yrhamnose polymer, with N-acetylglucosamine (GlcNAc) side chains, which is an essential virulence det

27 ction by attaching beta-N-acetylglucosamine (GlcNAc) to serine and threonine residues of intracellula

28 , we show that O-linked N-acetylglucosamine (GlcNAc) transferase (OGT), an enzyme that catalyzes O-Gl

29 of the Candida albicans N-acetylglucosamine (GlcNAc) transporter NGT1, and represents the first plasm

30 tennary glycan that has N-acetylglucosamine (GlcNAc), N-acetyllactosamine (LacNAc), and unnatural Gal

31 response to the inducer N-acetylglucosamine (GlcNAc), suggesting that a basal level of cAMP is suffic

32 ning host proteins with N-acetylglucosamine (GlcNAc), thereby blocking extrinsic apoptosis signaling.

33 ) type] terminated with N-acetylglucosamine (GlcNAc), which is generated by N-acetylglucosaminyltrans

34 teine residues bound to N-acetylglucosamine (GlcNAc).

35 at the 6-O-sulfation of N-acetylglucosamine (GlcNAc-6-O-sulfation) is highly conserved in PNS myelin

36 This synergy between alkalinization and GlcNAc to induce hyphal genes involves the Rim101 pH-sen

37 by the GlcNAc-phosphate transferase GacO and GlcNAc-phosphate-undecaprenol (GlcNAc-P-Und) produced by

38 alyzing the transfer of GlcNAc, Glc, Glc and GlcNAc residues to the protein backbone sequentially.

39 lyzing the transfer of GlcNAc, Glc, Glc, and GlcNAc residues to the protein backbone sequentially.

40 g protein (RBP) involved in this process and GlcNAc residues on WTA were found to be the key componen

41 impact on the substrate activity of another GlcNAc acceptor toward some endoglycosynthases in transg

42 ylation of N-glycans lacking an alpha1,3-arm GlcNAc in cells.

43 e N-glycans lacking an unmasked alpha1,3-arm GlcNAc moiety are not FUT8 substrates.

44 lation of N-glycans lacking the alpha1,3-arm GlcNAc moiety.

45 confirmed the predicted sugar identities as GlcNAc, Gal, and Fuc.

46 alpha-Rha-(1-->2)-alpha-Rha3OMe-(1-->3)-beta-GlcNAc-(1-->)Ser , and the novel capping moiety was show

47 ld be obtained by removal of a terminal beta-GlcNAc moiety by treatment with beta-N-acetylglucosamini

48 iate glycosidase to liberate a terminal beta-GlcNAc moiety, which can be converted into LacNAc and th

49 Next, the beta-GlcNAc terminating antenna can be converted into LacNAc

50 Ngs1 can bind GlcNAc through the N-terminal beta-N-acetylglucosaminida

51 vr4 share functional specificity in binding (GlcNAc)6 and in providing protection against plant- and

52 G glycan structures) and increased bisecting GlcNAc in IgG glycan structures were strongly associated

53 This indicates that conventional GlcNAc-mers are unlikely to be produced and/or accumulat

54 saccharide LacdiNAc (beta-d-GalNAc-[1-->4]-d-GlcNAc), which is associated with tumor malignancy in le

55 do-(2 --> 6)-beta-d-GlcNAc-(1 --> 6)-alpha-d-GlcNAc equipped with a 3-aminopropyl spacer moiety was p

56 -Kdo-(2 --> 4)-]alpha-d-Kdo-(2 --> 6)-beta-d-GlcNAc-(1 --> 6)-alpha-d-GlcNAc equipped with a 3-aminop

57 ha-L-Fuc-(1-->4)-[beta-D-Gal-(1-->3)]-beta-D-GlcNAc-(1-->3)-beta-D-Gal-(1-->4) -[alpha-L-Fuc-(1-->3)]

58 -D-Gal-(1-->4) -[alpha-L-Fuc-(1-->3)]-beta-D-GlcNAc-(1-->OR).

59 tabolic chemical reporter, 6-Alkynyl-6-deoxy-GlcNAc (6AlkGlcNAc), for the identification of O-GlcNAc-

60 Many fungi are able to utilize environmental GlcNAc to support growth and induce cellular development

61 re, we identify a gene that is essential for GlcNAc signalling (NGS1) in Candida albicans, a commensa

62 stantially exceed those usually measured for GlcNAc-binding lectins.

63 tyltransferase domain, which is required for GlcNAc-induced promoter histone acetylation and transcri

64 e Ngs1 as a GlcNAc-sensor and transducer for GlcNAc-induced transcription.

65 t enabling facile distinction of GlcNAc from GlcNAc with core fucose.

66 osyltransferase, GacL, transfers GlcNAc from GlcNAc-P-Und to polyrhamnose.

67 LDNF epitope [Fucalpha3GalNAcbeta4(Fucalpha3)GlcNAc-R], which is also recognized by the IgG monoclona

68 ubstrate specificity toward alpha1,6-fucosyl-GlcNAc-Asn or alpha1,6-fucosyl-GlcNAc-polypeptide in tra

69 ha1,6-fucosyl-GlcNAc-Asn or alpha1,6-fucosyl-GlcNAc-polypeptide in transglycosylation, enabling a hig

70 isomer at low level, terminal GlcNAc of G1F+GlcNAc, was identified to be linked at the 1,6 branch.

71 Mutants that elaborated 4- (Gal-GlcNAc-Gal-Glc-HepI) and 5-glycan (GalNAc-Gal-GlcNAc-Gal

72 lcNAc-Gal-Glc-HepI) and 5-glycan (GalNAc-Gal-GlcNAc-Gal-Glc-HepI) structures displayed intermediate p

73 ase, transferring GlcNAc residues to Glc-Glc-GlcNAc-modified Fap1.

74 ransferase, transferring Glc residues to Glc-GlcNAc-modified Fap1.

75 for the chitin degradation products GlcNAc, (GlcNAc)2 and (GlcN)2 , play in chitin utilization and co

76 agglutinin-detectable N-acetyl-glucosamine (GlcNAc) epitopes were not identified when the oomycete w

77 The monosaccharide N-acetyl-d-glucosamine (GlcNAc) is an abundant building block in naturally occur

78 of beta-1, 4-linked N-acetyl-D-glucosamine (GlcNAc).

79 approximately 35%), N-acetyl-d-glucosamine (GlcNAc)/GalNAc containing glycans recognized by the lect

80 One receptor binds the methyl glycoside GlcNAc-beta-OMe with Ka approximately 20,000 m(-1), wher

81 Ngs1 is conserved in diverse fungi that have GlcNAc catabolic genes.

82 These findings serve to explain how GlcNAc-1-phosphotransferase recognizes a large number of

83 Disparity in GlcNAc to ribitol connectivity, as well as variable O-ac

84 ecaprenol-linked GlcNAc-lipid intermediates: GlcNAc-pyrophosphoryl-undecaprenol (GlcNAc-P-P-Und) prod

85 fucose moiety specifically at the Asn-linked GlcNAc moiety not only to GlcNAc-peptide but also to hig

86 fucose from GDP-fucose to asparagine-linked GlcNAc of the N-glycan core in the medial Golgi.

87 rate that even addition of a single N-linked GlcNAc at potential glycosylation sites inhibits dimer f

88 is requires two distinct undecaprenol-linked GlcNAc-lipid intermediates: GlcNAc-pyrophosphoryl-undeca

89 DP-N-acetylglucosamine (UDP-GlcNAc),O-linked-GlcNAc transferase (OGT) catalyzes Ser/ThrO-GlcNAcylatio

90 T1, and represents the first plasma membrane GlcNAc transporter identified from plants.

91 acid-(beta-1,4)-N-acetylglucosamine (MurNAc-GlcNAc) disaccharides associated through cross-linked pe

92 From its crystal structures, N1574-GlcNAc is predicted to form stabilizing intradomain inte

93 emically modified nucleotide sugars UDP-4-N3-GlcNAc and UDP-4-N3-GalNAc were chemically synthesized f

94 UDP-4-N3-GlcNAc served as a chain termination substrate for hyalu

95 n or heparosan synthases; the resulting 4-N3-GlcNAc-terminated hyaluronan and heparosan were then suc

96 hat the protecting groups on one neighboring GlcNAc moiety have an impact on the substrate activity o

97 O-GlcNAc glycosylation (or O-GlcNAcylation) is a dynamic,

98 O-GlcNAc is a regulatory post-translational modification o

99 O-GlcNAc modification (O-GlcNAcylation) is required for su

100 O-GlcNAc transferase (OGT) catalyzes the posttranslational

101 O-GlcNAc transferase (OGT) is elevated in multiple cancers

102 O-GlcNAc transferase (OGT) regulates a wide range of cellu

103 O-GlcNAc transferase (OGT), the solo enzyme for O-GlcNAcyl

104 O-GlcNAc transferase (OGT/SXC) is essential for Pc repress

105 O-GlcNAc transferase is responsible for O-GlcNAc addition

106 s sequence for O-GlcNAcylation predicts 18 O-GlcNAc sites on Notch, we only observed apparent O-GlcNA

107 ycoproteomics approach, we identified >200 O-GlcNAc proteins in human T cells.

108 Moreover, it suggests that aberrant O-GlcNAc signaling can contribute to the development of ne

109 enzyme O-linked-beta-N-acetylglucosamine (O-GlcNAc) glycosyltransferase as compared with naive cells

110 ication O-linked beta-N-acetylglucosamine (O-GlcNAc) is a proposed nutrient sensor that has been show

111 on with O-linked beta-N-acetylglucosamine (O-GlcNAc) is one of the protein glycosylations affecting v

112 Although the O-linked N-acetylglucosamine (O-GlcNAc) modification of the RNA polymerase II C-terminal

113 ate that the O-linked N-acetylglucosamine (O-GlcNAc) processing enzymes, O-GlcNAc-transferase (OGT) a

114 ication O-linked beta-N-acetylglucosamine (O-GlcNAc) regulates thousands of nuclear, cytoplasmic, and

115 n of an O-linked beta-N-acetylglucosamine (O-GlcNAc) sugar moiety to hydroxyl groups of serine/threon

116 te that O-linked beta-N-acetylglucosamine (O-GlcNAc) transferase (OGT) is required for glucagon-stimu

117 sensor O-linked-beta-N-acetylglucosamine (O-GlcNAc) transferase (OGT) modifies intracellular protein

118 N-Acetylglucosamine (O-GlcNAc) transferase (OGT) regulates protein O-GlcNAcylat

119 ified by the O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT) SECRET AGENT (SEC) in Arabidop

120 residues by O-linked N-acetylglucosamine (O-GlcNAc).

121 impacts the epigenetic machinery allowing O-GlcNAc accumulation on RNA polymerase II and numerous ch

122 osophila allowing visualization of altered O-GlcNAc cycling on polytene chromosomes.

123 Microarray analysis suggested that altered O-GlcNAc cycling perturbed the expression of genes associa

124 NA pol II, SPT5, TRIM28-KAP1-TIF1beta, and O-GlcNAc itself.

125 n start site of MYBL1 were identified, and O-GlcNAc levels regulated their methylation status.

126 and approximately 43%, respectively), and O-GlcNAc protein modification.

127 events pol II entry into the promoter, and O-GlcNAc removal from pol II is an ATP-dependent step duri

128 ChIP-sequencing experiments using an anti-O-GlcNAc antibody revealed significant chromatin enrichmen

129 sites on Notch, we only observed apparent O-GlcNAc modification at five sites.

130 e genes encode enzymes for its attachment (O-GlcNAc transferase (OGT)) and removal (O-GlcNAcase (OGA)

131 tatarM/S, which lacks both alpha- and beta-O-GlcNAc residues on its wall teichoic acids (WTAs).

132 Beyond its well-known role in adding beta-O-GlcNAc to serine and threonine residues of nuclear and c

133 , and consistent with a connection between O-GlcNAc and RNA, inhibition of OGT impaired nascent RNA s

134 als exhibited dramatically increased brain O-GlcNAc levels and pleiotropic phenotypes, including earl

135 ttranslational modification of proteins by O-GlcNAc and is regulated by nutrient access.

136 -dependent signaling pathways regulated by O-GlcNAc glycosyltransferase are thus fundamental for T ce

137 oint genomic regions that are regulated by O-GlcNAc levels, we performed ChIP-chip and microarray ana

138 f Hippo pathway (YAP) is O-GlcNAcylated by O-GlcNAc transferase (OGT) at serine 109.

139 GlcNAc can be added to proteins by O-GlcNAc transferase (OGT) to regulate protein activity.

140 y, the tumor suppressor p53 is modified by O-GlcNAc, and most solid tumors contain mutations in p53 l

141 igenetic regulation of MYBL1 expression by O-GlcNAc, thereby significantly affecting tumor progressio

142 f colorectal adenocarcinoma progression by O-GlcNAc, we have focused on the O-GlcNAc-mediated epigene

143 In contrast, O-GlcNAc levels were strikingly insensitive to OGA RNAi at

144 onal health and suggest that dysfunctional O-GlcNAc signaling may be an important contributor to neur

145 he majority of genes regulated by elevated O-GlcNAc levels are similarly regulated by a shift from eu

146 Cells with elevated O-GlcNAc levels had elongated mitochondria and increased m

147 te that oxidative stress leads to elevated O-GlcNAc levels in U2OS cells but has little impact on the

148 Moreover, elevated O-GlcNAc levels promoted weight loss and lowered respirati

149 s to be, at least in part, due to elevated O-GlcNAc-dependent increases in Ins1 and Ins2 mRNA levels

150 Type II diabetic patients have elevated O-GlcNAc-modified proteins within pancreatic beta cells du

151 ression of the O-GlcNAc-regulating enzymes O-GlcNAc transferase (OGT) or O-GlcNAcase (OGA) impairs mi

152 glucosamine (O-GlcNAc) processing enzymes, O-GlcNAc-transferase (OGT) and O-GlcNAcase (OGA), interact

153 ng up to five monosaccharides are extended O-GlcNAc's rather than GalNAc-initiated O-glycans.

154 O-GlcNAc transferase is responsible for O-GlcNAc addition to serine and threonine (Ser/Thr) residu

155 of a family of complementary receptors for O-GlcNAc in different contexts.

156 in cancer and suggests a crucial role for O-GlcNAc signaling in transducing nutritional state to reg

157 glucose overload, but a molecular role for O-GlcNAc within beta cells remains unclear.

158 , we discovered the presence of functional O-GlcNAc transferase (OGT), O-GlcNAcase (OGA), and nucleoc

159 l consequences of histone O-GlcNAcylation (O-GlcNAc=O-linked beta-N-acetylglucosamine) are largely un

160 th patient-derived fibroblasts, but global O-GlcNAc levels appeared to be unaffected.

161 ells, we observed that steady-state global O-GlcNAc levels remained grossly unaltered.

162 lation.O-linked beta-N-acetyl glucosamine (O-GlcNAc) is an important protein modification that is hyd

163 The O-linked beta-N-acetyl glucosamine (O-GlcNAc) modification dynamically regulates the functions

164 These data suggest that changes in O-GlcNAc homeostasis activate the p53 pathway.

165 In conclusion, changes in O-GlcNAc homeostasis activate the wild type p53 pathway in

166 We conclude that defects in O-GlcNAc homeostasis and host cell factor 1 proteolysis ma

167 ing adaptability and specificity to OGA in O-GlcNAc regulation.O-linked beta-N-acetyl glucosamine (O-

168 activity, we show that acutely increasing O-GlcNAc levels can significantly attenuate ongoing epilep

169 Interestingly, O-GlcNAc levels and NRF2 activation co-vary in response to

170 diabetic rats show increased mitochondrial O-GlcNAc transferase (OGT) and a concomitant decrease in t

171 CCSC compartment observed after modulating O-GlcNAc levels is therefore likely to result, at least in

172 ome-wide increase in the intensity of most O-GlcNAc-occupied regions including genes linked to cell c

173 in vivo by introducing a dominant negative O-GlcNAc transferase mutant (F460A) restored Ogg1 enzymati

174 ine, we demonstrate that elevating nuclear O-GlcNAc increases intracellular insulin levels and preser

175 es our current understanding of changes of O-GlcNAc cycling enzymes in cancer, the role of O-GlcNAcyl

176 e in the mouse brain to define the role of O-GlcNAc cycling in the central nervous system.

177 gulation of elongation by the insertion of O-GlcNAc cycling into the pol II elongation regulatory dyn

178 , we performed a comprehensive analysis of O-GlcNAc during T cell activation to address the functiona

179 , our studies provide a global analysis of O-GlcNAc dynamics during T cell activation and the first c

180 the TCR resulted in a global elevation of O-GlcNAc levels and in the absence of O-GlcNAc, IL-2 produ

181 In addition, modulation of O-GlcNAc levels was demonstrated to be important during th

182 ontaining AMPARs, similar to expression of O-GlcNAc LTD.

183 The acquisition of O-GlcNAc signaling by metazoa may have facilitated the rap

184 horylation and establish the importance of O-GlcNAc signaling in coupling liver autophagy to nutrient

185 ICANCE STATEMENT We show the importance of O-GlcNAc transferase (OGT) for sensory neuron health and s

186 xpectedly, many transcriptional effects of O-GlcNAc transferase (OGT) inhibition were due to the acti

187 d to changes in the relative expression of O-GlcNAc transferase (OGT) isoforms and accumulation of OG

188 Loss of O-GlcNAc transferase blocked T cell progenitor renewal, ma

189 n of O-GlcNAc levels and in the absence of O-GlcNAc, IL-2 production and proliferation were compromis

190 vealed significant chromatin enrichment of O-GlcNAc-modified proteins at the promoter of the transcri

191 Ac (6AlkGlcNAc), for the identification of O-GlcNAc-modified proteins.

192 hion within the transferase active site of O-GlcNAc-transferase (OGT).

193 exists on promoters in vitro Inhibition of O-GlcNAc-transferase activity and O-GlcNAcylation prevents

194 f-renewal of CCSC due to reduced levels of O-GlcNAc.

195 the observed stress-induced elevations of O-GlcNAc.

196 peptides with O-GalNAc (the Tn antigen) or O-GlcNAc, we demonstrated that the method is selective for

197 phosphorylates OGT, which in turn promotes O-GlcNAc modification and activation of Ulk proteins by po

198 The nutrient sensing protein O-GlcNAc transferase (OGT) mediates post-translational O-l

199 of the metabolic/nutrient sensing protein O-GlcNAc transferase that mediates the O-linked addition o

200 eonine residues of intracellular proteins (O-GlcNAc), regulates food intake by modulating excitatory

201 icted O-glucose sites, and all 18 putative O-GlcNAc sites.

202 llowing us to predict hundreds of putative O-GlcNAc transferase (OGT) substrates.

203 ase (OGA), the enzymes that add and remove O-GlcNAc, respectively, are regulated during oxidative str

204 copeptide substrates that contain a single O-GlcNAc modification on a serine or threonine residue.

205 lycopeptide substrates containing a single O-GlcNAc modification on either a serine or threonine.

206 cted individuals, to maintain steady-state O-GlcNAc levels.

207 a search for a reductionist model to study O-GlcNAc signaling, we discovered the presence of function

208 Sustained O-GlcNAc elevation in SH-SY5Y neuroblastoma cells increase

209 epression at hippocampal CA3-CA1 synapses (O-GlcNAc LTD).

210 s a novel form of LTD at CA3-CA1 synapses, O-GlcNAc LTD.

211 Given that O-GlcNAc appears to regulate cell signaling pathways and p

212 These results strongly argue that O-GlcNAc epigenetically regulates MYBL1, functioning simil

213 increased CCSC population, indicating that O-GlcNAc levels regulated the CCSC compartment.

214 We have previously discovered that O-GlcNAc transferase (OGT), an enzyme that modifies protei

215 These data indicate that O-GlcNAc-transferase activity is essential for RNA pol II

216 characterization, to our knowledge, of the O-GlcNAc glycoproteome in human T cells.

217 These findings implicate the O-GlcNAc modification as a potential mechanism for hypergl

218 The O-GlcNAc modification is present on numerous nuclear and c

219 These findings link the O-GlcNAc modification to mammalian neurogenesis and highli

220 repeat domain) of OGT, which catalyzes the O-GlcNAc post-translational modification of nuclear and cy

221 ular processes through the addition of the O-GlcNAc sugar moiety to thousands of protein substrates.

222 The mechanisms by which the O-GlcNAc transferase (OGT) and the O-GlcNAcase (OGA), the

223 Deletion of the O-GlcNAc transferase (ogt) gene responsible for the modifi

224 ession by O-GlcNAc, we have focused on the O-GlcNAc-mediated epigenetic regulation of human colon can

225 O-GlcNAcylation) via overexpression of the O-GlcNAc-regulating enzymes O-GlcNAc transferase (OGT) or

226 OGT transfers O-GlcNAc onto serine and threonine residues in intrinsical

227 g site-specific single, double, and triple O-GlcNAc and phosphomutants of K18 were used to identify t

228 ember SET1 histone methyltransferases were O-GlcNAc-modified in oga(del.1) mutants.

229 ore, we show that Mi2beta is modified with O-GlcNAc, and both OGT and OGA interact with Mi2beta, GATA

230 detail the synthesis and characterization of GlcNAc-BABS, revealing a striking 99.9% quenching effici

231 ons imply about the absolute conservation of GlcNAc as the monosaccharide through which N-linked glyc

232 igh content of GlcN (30%) and low content of GlcNAc (4.2%) determined by disaccharide composition ana

233 ide component enabling facile distinction of GlcNAc from GlcNAc with core fucose.

234 on with a traditional thioglycoside donor of GlcNAc, which otherwise affords poor glycosylation yield

235 variable O-acetylation and glycosylation of GlcNAc contribute to the structural diversity of WTAs.

236 Loss of GlcNAc-1-phosphotransferase results in hydrolase hyperse

237 Ngs1 is targeted to the promoters of GlcNAc-inducible genes constitutively by the transcripti

238 A key property of GlcNAc-1-phosphotransferase is its unique ability to dis

239 The acetylation state of GlcNAc did not affect linkage.

240 p1 glycosylation, catalyzing the transfer of GlcNAc, Glc, Glc and GlcNAc residues to the protein back

241 p1 glycosylation, catalyzing the transfer of GlcNAc, Glc, Glc, and GlcNAc residues to the protein bac

242 that AnCDA catalyses mono-deacetylation of (GlcNAc)2 and full deacetylation of (GlcNAc)3-6 in a non-

243 tion of (GlcNAc)2 and full deacetylation of (GlcNAc)3-6 in a non-processive manner.

244 he GAC polyrhamnose backbone is assembled on GlcNAc-P-P-Und.

245 enes involves the Rim101 pH-sensing pathway; GlcNAc induced rim101Delta and dfg16Delta mutants to for

246 nt as substrate (GlcNAc-MurNAc(pentapeptide)-GlcNAc-MurNAc(pentapeptide)).

247 ymeN-acetylglucosamine-1-phosphotransferase (GlcNAc-1-phosphotransferase), an alpha2beta2gamma2hexame

248 ne and degrade chitin substrates to produce (GlcNAc)2, a source of carbon, nitrogen and energy.

249 ely degrades chitin substrates and produces (GlcNAc)2 fragments in the mouse gastrointestinal environ

250 systems for the chitin degradation products GlcNAc, (GlcNAc)2 and (GlcN)2 , play in chitin utilizati

251 es introduction of distinguishably protected GlcNAc-Asn building blocks during automated solid phase

252 ans with more sugar residues on the proximal GlcNAc than previously resolved.

253 glycan structure is the first sugar residue (GlcNAc) at the N1574 attachment site.

254 ults show that glycoproteins modified with S-GlcNAc are mainly involved in cell-cell adhesion and gen

255 ectodomains further showed that at least six GlcNAc moieties (CO6) are required for optimal binding e

256 a small synthetic PG fragment as substrate (GlcNAc-MurNAc(pentapeptide)-GlcNAc-MurNAc(pentapeptide))

257 uch structural isomer at low level, terminal GlcNAc of G1F+GlcNAc, was identified to be linked at the

258 , preferring to transfer GlcNDAz rather than GlcNAc to protein substrates.

259 dditionally, adsorption assays indicate that GlcNAc residues on WTAs and O-acetyl groups at the 6-pos

260 pe carbohydrate recognition domains, and the GlcNAc and galactose residues make additional interactio

261 of a 1,6 glycosidic bond between CPS and the GlcNAc C-6.

262 ndecaprenol (GlcNAc-P-P-Und) produced by the GlcNAc-phosphate transferase GacO and GlcNAc-phosphate-u

263 However, how the GlcNAc signal is sensed and subsequently transduced is l

264 , followed by orthogonal deprotection of the GlcNAc primers and site-selective sequential extension o

265 , to a minor extent, to the back-face of the GlcNAc sugar ring.

266 mannose 6-phosphate tag by the action of the GlcNAc-1-phosphotransferase enzyme, allowing them to bin

267 n and myelinated axonal survival through the GlcNAc-6-O-sulfation of N-glycans on glycoproteins.

268 f the M6P moieties and their transfer to the GlcNAc-protein by an endoglycosynthase to provide homoge

269 ound that proteins were extensively bound to GlcNAc through the side chains of cysteine residues in h

270 In C. albicans, exposure to GlcNAc activates cell signalling and virulence.

271 at the Asn-linked GlcNAc moiety not only to GlcNAc-peptide but also to high-mannose and complex-type

272 a distinct glycosyltransferase, transferring GlcNAc residues to Glc-Glc-GlcNAc-modified Fap1.

273 a GT-C glycosyltransferase, GacL, transfers GlcNAc from GlcNAc-P-Und to polyrhamnose.

274 lycan features (i.e. occupancy, triantennary GlcNAc branching, and alpha1,6-fucosylation) and augment

275 -95 carries a core glycan, consisting of two GlcNAc and three hexoses.

276 UDP-GlcNAc is the donor substrate used in multiple glycosyla

277 key catalytic domain residues and even a UDP-GlcNAc oxygen important for Ser/Thr glycosylation are ir

278 ently shown, unexpectedly, to occur in a UDP-GlcNAc-dependent fashion within the transferase active s

279 se motif with alanine residues abolished UDP-GlcNAc binding and lymphostatin activity, although other

280 uridine diphosphate-N-acetylglucosamine (UDP-GlcNAc) but not UDP-glucose (UDP-Glc).

281 HBP metabolite UDP-N-acetylglucosamine (UDP-GlcNAc) to CRPC-like cells significantly decreases cell

282 uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), a substrate for cellular glycosyltransferases.

283 the cosubstrate UDP-N-acetylglucosamine (UDP-GlcNAc),O-linked-GlcNAc transferase (OGT) catalyzes Ser/

284 uridine diphosphate-N-acetylglucosamine (UDP-GlcNAc).

285 The Golgi enzyme UDP-GlcNAc:lysosomal enzymeN-acetylglucosamine-1-phosphotran

286 c) units within N-glycans initiated from UDP-GlcNAc by the medial-Golgi branching enzymes as well as

287 ly 2-5% of the total glucose, generating UDP-GlcNAc as the end product.

288 GNE (UDP-GlcNAc 2-epimerase/ManNAc kinase) myopathy is a rare mus

289 cells contained higher concentrations of UDP-GlcNAc and increased intracellular protein O-GlcNAcylati

290 GNE deficiency may affect levels of UDP-GlcNAc, a key metabolite in the nutrient-sensing hexosam

291 e and glutamine for de novo synthesis of UDP-GlcNAc, a sugar-nucleotide that inhibits receptor endocy

292 by the lack of ROCK1-mediated supply of UDP-GlcNAc.

293 sensing hexosamine biosynthetic pathway, UDP-GlcNAc, as its substrate donor.

294 and glutaminolysis co-operatively reduce UDP-GlcNAc biosynthesis and N-glycan branching in mouse T ce

295 is triggered by redistribution of unused UDP-GlcNAc from the medial to trans-Golgi via inter-cisterna

296 catalytic domains, which, together with UDP-GlcNAc, are required for both glycosylation and proteoly

297 rase GacO and GlcNAc-phosphate-undecaprenol (GlcNAc-P-Und) produced by the glycosyltransferase GacI.

298 ediates: GlcNAc-pyrophosphoryl-undecaprenol (GlcNAc-P-P-Und) produced by the GlcNAc-phosphate transfe

299 nges of performing direct glycosylation with GlcNAc.

300 mechanism of polyrhamnose modification with GlcNAc are currently unknown.