ライフサイエンスコーパス: glucosamine

1 on product, UDP-(3-O-(R-3-hydroxymyristoyl))-glucosamine.

2 the polysaccharide poly beta-1,6-N-acetyl-d-glucosamine.

3 sphate, the intracellular form of N-acetyl-D-glucosamine.

4 UDP-ManNAc3NAcA starting from UDP-N-acetyl-d-glucosamine.

5 aminoquinoline and naphthalimide moieties by glucosamine.

6 omposing the unit as rhamnose and N-acetyl-D-glucosamine.

7 ot observed with equimolar concentrations of glucosamine.

8 to the inhibition of Th1 differentiation by glucosamine.

9 a functional competition between glucose and glucosamine.

10 nce the exchange rate of the nearby N-acetyl glucosamines.

11 human articular cartilage were treated with glucosamine (0.1- 10 mM).

12 essential for bacterial growth, converting D-glucosamine 1-phosphate into UDP-GlcNAc via acetylation

13 leophilicity of the attacking amino group of glucosamine 1-phosphate.

14 s [-4) beta-L-rhamnose (1-3) beta-N-acetyl-D-glucosamine (1-] with an N-acetyl-D-glucosamine nonreduc

15 01 protein catalyzed both the acetylation of glucosamine-1-phosphate and the uridylyltransferase reac

16 N-acetyl-glucosamine-1-phosphate uridyltransferase (GlmU), a bifu

17 two activator muropeptides, N-acetyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-d-muramyl-

18 eport the total syntheses of N-acetyl-beta-D-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-D-muramyl-

19 gram-negative bacteria) and N-acetyl-beta-D-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-D-muramyl-

20 zyme catalyzes hydrolysis of N-acetyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-d-muramyl-

21 This product, an N-acetyl-beta-D-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-D-muramylp

22 ified in response to high glucose (20 mm) or glucosamine (10 mm) treatment, suggesting differential t

23 trations were associated with regular use of glucosamine (17%, 95% confidence interval (CI): 7, 26),

24 thyl-(2-fluoroethyl)-1H-[1,2,3]triazole-4-yl)glucosamine ((18)F-NFTG) annotates glycogenesis in cance

25 ine-phosphatidylinositol (glucosamine-PI) or glucosamine 2-O-methyl inositol octadecyl phosphate, red

26 First, the sulfate analogue, d-glucosamine 2-sulfate, acted as a non-transported agonis

27 eta-d-muramyl-peptide (1) to N-acetyl-beta-d-glucosamine (2) and 1,6-anhydro-N-acetyl-beta-d-muramyl-

28 g that CsaA is the functional UDP-N-acetyl-D-glucosamine-2-epimerase and CsaB the functional poly-Man

29 -C are thought to encode the UDP-N-acetyl-D-glucosamine-2-epimerase, poly-ManNAc-1-phosphate-transfe

30 and during the resuscitation phase received glucosamine (270 mg/kg) to increase O-GlcNAc synthesis o

31 s directly regulated by heparan sulfate (HS) glucosamine 3-O-sulfotransferase 3B1 (HS3ST3B1).

32 al arylsulfatase G (ARSG) is the long-sought glucosamine-3-O-sulfatase required to complete the degra

33 th the peracetylated 4-fluorinated analog of glucosamine (4-F-GlcNAc) elicits anti-skin inflammatory

34 d analogue of glucosamine (4-fluoro-N-acetyl-glucosamine (4-F-GlcNAc)) on the synthesis of heparan su

35 oma-bearing mice with peracetylated 4-fluoro-glucosamine (4-F-GlcNAc), a metabolic inhibitor of N-ace

36 ingly, we tested the fluorinated analogue of glucosamine (4-fluoro-N-acetyl-glucosamine (4-F-GlcNAc))

37 he 5 groups in the GAIT continued to receive glucosamine 500 mg 3 times daily, CS 400 mg 3 times dail

38 UGlcNAcDH encodes a UDP-N-acetyl-glucosamine 6-dehydrogenase, converting UDP-N-acetylgluc

39 er cell lines results in 30-50% reduction in glucosamine 6-O-sulfate levels in HS, impairing HB-EGF-d

40 xtracellular sulfatases that act on internal glucosamine 6-O-sulfate modifications within heparan sul

41 was indispensable for both arylsufatase and glucosamine 6-O-sulfate-endosulfatase activity.

42 lays high levels of HS sequences that harbor glucosamine 6-O-sulfates when compared with normal ovari

43 e that heparin-induced leukocytosis requires glucosamine 6-O-sulfation and is caused by blockade of L

44 ozyme in states before the activating sugar, glucosamine 6-phosphate (GlcN6P), has bound and after th

45 he glmS ribozyme, is adapted to an assay for glucosamine 6-phosphate, an effector molecule for the ap

46 e wild-type enzyme, alone or in complex with glucosamine 6-phosphate, are also consistent with a hexa

47 the hexameric form in the presence of cyclic glucosamine 6-phosphate, together with the decrease of t

48 in the ubiquitous metabolites glycolate and glucosamine 6-phosphate.

49 g glucose 6-phosphate, MondoA can also sense glucosamine 6-phosphate.

50 ice markedly overexpress the heparan sulfate glucosamine-6-O-endosulfatase-2 (SULF2), an enzyme that

51 disrupt HSPG structure: the heparan sulfate glucosamine-6-O-endosulfatase-2 (Sulf2).

52 The d-glucosamine-6-phosphate (GlcN6P) cofactor has been propo

53 tive bacteria and is located upstream of the glucosamine-6-phosphate (GlcN6P) synthetase reading fram

54 Binding of glucosamine-6-phosphate (GlcN6P) uncovers the latent sel

55 th the assistance of the metabolite cofactor glucosamine-6-phosphate (GlcN6P), whose amino group is p

56 Two analogues of glucosamine-6-phosphate (GlcN6P, 1) and five of glucosam

57 ccur by an acid-base mechanism involving the glucosamine-6-phosphate cofactor and G40 residue.

58 ), phosphofructokinase (PfkB, but not PfkA), glucosamine-6-phosphate deaminase (NagB), and adenylate

59 The amino-terminal cysteine of glucosamine-6-phosphate synthase (GlmS) acts as a nucleo

60 rtion in glmS, encoding the essential enzyme glucosamine-6-phosphate synthase that catalyzes the firs

61 gC is relieved in the presence of N-acetyl-D-glucosamine-6-phosphate, the intracellular form of N-ace

62 monstrate here that 6-azido-6-deoxy-N-acetyl-glucosamine (6AzGlcNAc) is a specific MCR for O-GlcNAcyl

63 galactosamine derivatives, N-thioglycolyl-D-glucosamine (7, C-4 epimer of 1), and alpha-O-benzyl 2-a

64 is also shown to be the first characterized glucosamine ABC transporter.

65 sis root and that SPINDLY (SPY), an O-linked glucosamine acetyltransferase, regulates cortex prolifer

66 sferase (LpxA) and UDP-3-O-(R-3-hydroxyacyl)-glucosamine acyltransferase (LpxD) catalyze the first an

67 ne acyltransferase (LpxA) and UDP-3-O-(acyl)-glucosamine acyltransferase (LpxD) constitute the essent

68 ynthesis driven by HAS2 was less affected by glucosamine addition, and HAS3 was not affected at all.

69 y and reduced uridine diphosphate-N-acetyl-D-glucosamine, along with decreased O- and N-linked protei

70 hat it was PNAG, but notably only 60% of the glucosamine amino groups were acetylated.

71 response to glucose are mimicked by N-acetyl glucosamine, an intermediate of the hexosamine biosynthe

72 ctively expose the 6-OH group in N-protected glucosamine analogues, which provided another route to c

73 95% CI: 0.72, 0.97; P for trend = 0.009) for glucosamine and 0.83 (95% CI: 0.69, 1.00; P for trend =

74 NMR characterization of the amine groups of glucosamine and 3-O-sulfoglucosamine in aqueous solution

75 ucleocytoplasmic proteins with beta-N-acetyl-glucosamine and a process regulated by glucose metabolis

76 Glucosamine and allosamine with 3-azido substitutions we

77 udy was undertaken to evaluate the effect of glucosamine and chondroitin sulfate (CS), alone or in co

78 These results suggest that glucosamine and chondroitin supplements are associated w

79 the nonvitamin-nonmineral supplements, only glucosamine and chondroitin were associated with total m

80 CS 400 mg 3 times daily, the combination of glucosamine and CS, celecoxib 200 mg daily, or placebo o

81 nd sodium acetate as well as by N-acetylated glucosamine and galactosamine (GlcNAc and GalNAc) and gl

82 This new method has been applied to both D-glucosamine and galactosamine trichloroacetimidate donor

83 lation with C(2)-N-substituted benzylidene D-glucosamine and galactosamine trichloroacetimidates.

84 ain saccharide component, with low levels of glucosamine and galacturonic acid also present.

85 inear polysaccharide of alternating N-acetyl-glucosamine and glucuronic acid residues, is ubiquitousl

86 CAM), 1-deoxy-1-aminomannopyranoside (DAMP), glucosamine and low molecular weight chitosan bonded to

87 o-glucuronic acid and propargyluted N-acetyl glucosamine and N-acetyl galactosamine derivative, respe

88 (D)-Glucosamine and other nutritional supplements have emerg

89 Both glucosamine and PUGNAc increased 24-hr survival compared

90 id A consists of two phosphorylated N-acetyl glucosamine and several acyl chains that are directly li

91 Glucosamine and thiamet-G also inhibited SOCE and were a

92 exhibited MS/MS fragmentations identical to glucosamine and those originating form aldohexoses showe

93 ted polysaccharide consisting of alternating glucosamine and uronic acid monosaccharide residues.

94 Use of glucosamine and use of chondroitin were each associated

95 Viosamine, together with rhamnose, (N-acetyl)glucosamine, and glucose, was found as a major component

96 endent N-acylation of UDP-3-O-(acyl)-alpha-D-glucosamine, and is a target for new antibiotic developm

97 ch as alloxan, D-glucosamine, and N-acetyl-D-glucosamine, and mimicked by the non-metabolizable gluco

98 by glucokinase inhibitors such as alloxan, D-glucosamine, and N-acetyl-D-glucosamine, and mimicked by

99 ffected by glucokinase inhibitors alloxan, d-glucosamine, and N-acetyl-d-glucosamine; and 4) orexin g

100 orted sugars, including glucose, xylose, and glucosamine, and this substrate-induced expression can b

101 itors alloxan, d-glucosamine, and N-acetyl-d-glucosamine; and 4) orexin glucosensors detect mannose,

102 ing the oral bioavailability of N-acetyl-(d)-glucosamine as its putative bioactive phosphate form wer

103 Numerous biomolecules possess alpha-D-glucosamine as structural component.

104 ontaining amide and urea derivatives using D-glucosamine as the starting material.

105 of HA, UDP-Glucuronic acid and UDP-N-Acetyl-Glucosamine, as well as hyaluronic acid synthase which f

106 nt probe for real-time detection of cellular glucosamine at micromolar level in living Caco-2 cells i

107 ase (NAT) Orf11*/Dbv8 through N-acylation on glucosamine at the central residue of Tei/A40926 pseudoa

108 zed for compositional analysis, 3-O-sulfated glucosamine at the reducing ends appears to be susceptib

109 fically degrades HS chains with 3-O-sulfated glucosamine at the reducing-end.

110 We describe metabolically inert l-glucosamine-based glycosylated antitumor ether lipids (L

111 bacteria contain lipopolysaccharide (LPS), a glucosamine-based phospholipid, in the outer leaflet of

112 ated by lipopolysaccharides (LPS), which are glucosamine-based phospholipids that form the outer leaf

113 3 and O-4 phosphate prodrugs of N-acetyl-(d)-glucosamine bearing a 4-methoxy phenyl group and differe

114 linear homopolymer poly-beta-1,6-N-acetyl-D-glucosamine (beta-1,6-GlcNAc; PGA) serves as an adhesin

115 lucose deprivation was blocked completely by glucosamine, but not by inhibition of OGA with 2-acetami

116 we show that the N-sulfate or 6-O-sulfate of glucosamine, but not the 2-O-sulfate of iduronate within

117 cose hexoses, allose, 3-O-methylglucose, and glucosamine by accumulating in the nucleus and activatin

118 reasing the cellular content of UDP-N-acetyl glucosamine by approximately 10-fold with 1 mm glucosami

119 ctive of this study was to determine whether glucosamine can activate autophagy.

120 nally protected derivatives of carba-alpha-D-glucosamine, carba-alpha-D-mannose, carba-alpha-D-mannur

121 ves the linkage of glucuronic acid linked to glucosamine carrying 6-O-sulfo groups.

122 glucuronic acid (or iduronic acid) linked to glucosamine carrying various sulfo groups.

123 -uptake channel EcChiP for processing by the glucosamine catabolic pathway.

124 es of 13 vitamin and mineral supplements and glucosamine, chondroitin, saw palmetto, Ginko biloba, ga

125 avages, as well as cross-ring and inter-ring glucosamine cleavages, compared to CID and IRMPD, becaus

126 A five-step transformation of D-glucosamine, commencing with indium-mediated Barbier rea

127 Accurate quantification of glucosamine content in chitin and chitosan with differen

128 NAD-ME affected both the amino acid and the glucosamine content of mid-veins.

129 ent transfer of a fatty acyl moiety to a UDP-glucosamine core ring.

130 is altered glycoform revealed an increase in glucosamine deposition.

131 Two urea-based receptors containing a glucosamine derivative were synthesized and investigated

132 strategies for elucidating the structures of glucosamine-derived sulfoforms with identical m/ z ratio

133 y develop insulin resistance when exposed to glucosamine, despite their "young" phenotype.

134 x10(4) and 1.45x10(4)M(-)(1), along with the glucosamine detection limits of 1.06 and 0.29microM are

135 In these lipid A samples the glucosamine disaccharide characteristic for enterobacter

136 The glucosamine disaccharide-as a backbone surrogate of the

137 transfers a C14:0 to the 2'-position of the glucosamine disaccharide.

138 acylating lipid A at the 2'-position of the glucosamine disaccharide.

139 characterized biofilm factors poly-N-acetyl glucosamine, fibronectin-binding proteins, or autolytic

140 hase synthesis with immobilised L-thyroxine, glucosamine, fumonisin B2 or biotin as template, can dem

141 We engineered a novel polymer, glucosamine-functionalized polyisobutylene-maleic acid,

142 ed disaccharide D-glucuronic acid-acetylated glucosamine (GlcA-GlcNAc).

143 s hydrolysed with Alcalase and glycated with glucosamine (GlcN) at moderate temperatures (37/50 degre

144 vealed that ArnT is required for addition of glucosamine (GlcN) to B. bronchiseptica lipid A.

145 old water fish skin gelatin hydrolysates and glucosamine (GlcN) via transglutaminase (TGase), as well

146 the 1- and 4'-phosphates by the addition of glucosamine (GlcN), whereas 18-323 cannot, and 2) the C3

147 GLUT2 can transport the amino sugar glucosamine (GlcN), which could increase substrate for t

148 tructural components such as N-unsubstituted glucosamine (GlcN).

149 cosamine-6-phosphate (GlcN6P, 1) and five of glucosamine (GlcN, 2) were prepared for evaluation as ca

150 Glucosamine (GlcN, 5% w/v) was incubated in either phosp

151 parameters for the deacetylation of N-acetyl-glucosamine (GlcNAc) by MshB, and the results from these

152 n the glycans D-mannose (Man) and D-N-acetyl glucosamine (GlcNAc) by the enzyme variants could then b

153 smic proteins by the monosaccharide N-acetyl-glucosamine (GlcNAc) continues to emerge as an important

154 r, wheat germ agglutinin-detectable N-acetyl-glucosamine (GlcNAc) epitopes were not identified when t

155 The monosaccharide N-acetyl-d-glucosamine (GlcNAc) is an abundant building block in na

156 of the group A carbohydrate, N-acetyl-beta-D-glucosamine (GlcNAc), and heart valve endothelium, lamin

157 (PGM3) catalyzes the conversion of N-acetyl-glucosamine (GlcNAc)-6-phosphate into GlcNAc-1-phosphate

158 e (GalNAc) in a beta-1,3 linkage to N-acetyl glucosamine (GlcNAc).

159 rom the F17 pilus that recognizes n-acetyl-d-glucosamine (GlcNAc).

160 in, a polymer of beta-1, 4-linked N-acetyl-D-glucosamine (GlcNAc).

161 charides of D-glucuronic acid and N-acetyl-D-glucosamine (GlcNAc).

162 an sulfate by approximately 35%), N-acetyl-d-glucosamine (GlcNAc)/GalNAc containing glycans recognize

163 cetyglucosamine (GlcNAz) and N-(4-pentynoyl)-glucosamine (GlcNAl) into cell-surface glycans and secre

164 ive proteomics with 6AzGlcNAc, N-azidoacetyl-glucosamine (GlcNAz), and N-azidoacetyl-galactosamine (G

165 sulfation of the 3-OH position of N-sulfated glucosamine (GlcNS) is the most beneficial modification

166 O-linked-N-acetyl-glucosamine glycosylation (O-GlcNAcylation) of the serin

167 1, PUGNAc: 357 +/- 99 IU, p < .05); however, glucosamine had no effect on these serum parameters.

168 Glucosamine has immunomodulatory effects on autoimmune d

169 le synthesis requires the precursor N-acetyl-glucosamine; however, capsule is synthesized during post

170 Four hexosamine monomer derivatives-glucosamine hydrochloride, glucosamine sulfate, galactos

171 We demonstrate that glucosamine impedes Th1, Th2, and iTreg but promotes Th1

172 ho-2-aminoglucolactam (31) was prepared from glucosamine in a 13-step synthesis, which included a lat

173 Actomyosin was conjugated with glucose or glucosamine in a liquid system at moderate temperatures

174 ifically removes the 6-O sulphate group from glucosamine in highly sulfated regions of HS chains.

175 , which perform sulfation at 6-O position in glucosamine in HS, impact ovarian cancer angiogenesis th

176 d motivate future studies on the efficacy of glucosamine in modifying aging-related cellular changes

177 erent peptidoglycans and to chitin, and that glucosamine in the glycan chains is the minimal binding

178 ucosamine by approximately 10-fold with 1 mm glucosamine in the growth medium.

179 into total ECM protein and collagen, by (3)H-glucosamine incorporation into chondroitin sulfate, kera

180 ost amino acids, similar ones were found for glucosamine, indicating that this amino sugar is release

181 ion of HBP, through the systemic infusion of glucosamine, induced severe insulin resistance (36% decl

182 catalyzes the ATP-dependent condensation of glucosamine-inositol (GlcN-Ins) and cysteine to form Cys

183 ily produce mycothiol (MSH or acetylcysteine-glucosamine-inositol, AcCys-GlcN-Ins) to protect the org

184 After being conjugated with the glucosamine, insulin can efficiently bind to RBC membran

185 Taken together, our results indicate that glucosamine interferes with N-glycosylation of CD25, and

186 parin were the hexuronic acid ion (m/z 175), glucosamine ion (m/z 240), and the disaccharide ion (m/z

187 These findings suggest that glucosamine is an effective autophagy activator and shou

188 Glucosamine is an important constituent of the heterogen

189 ial growth when the availability of N-acetyl-glucosamine is limited.

190 Chitin, a polymer of N-acetyl-d-glucosamine, is found in fungal cell walls but not in pl

191 noses, as exemplified by an application to D-glucosamine, is outlined.

192 Furthermore, PUGNAc but not glucosamine maintained O-GlcNAc levels in liver and lung

193 These effects suggest that glucosamine may be an important modulator of T cell diff

194 MVIC incorporations of (3)H-proline and (3)H-glucosamine, measures of extracellular matrix collagen a

195 This was associated with glucosamine-mediated inhibition of the Akt/FoxO3/mammali

196 Interestingly, excess glucose rescued this glucosamine-mediated regulation, suggesting a functional

197 However, the mechanism(s) through which glucosamine modulates different T cell subsets and disea

198 Glucosamine modulates molecular targets of the autophagy

199 ugh, modifies its lipid A by the addition of glucosamine moieties that promote TLR4 activation in hum

200 ther 0.1 or 0.25 degrees of substitution per glucosamine monomer.

201 ry, the binding stoichiometry of 2 and 1 for glucosamine monosaccharide (GlcN) and disaccharide (GlcN

202 cations consisting of an N-linked N-acetyl-D-glucosamine monosaccharide (N-GlcNAc).

203 of later-in-life MetS included citric acid, glucosamine, myoinositol, and proline (P < 0.03).

204 es annotated as UDP-3-O-[3-hydroxymyristoyl] glucosamine N-acyltransferase genes (la0512 and la4326 [

205 hat the signal for position 2 of trisulfated glucosamine [N-, 3-O-, and 6-O-sulfated] (A*) is bifurca

206 s observed with other sugars like N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-glucose and D-g

207 acetyl-D-glucosamine (1-] with an N-acetyl-D-glucosamine nonreducing terminus.

208 ondrial proteins by O-linked beta-N-acetyl-D-glucosamine (O-GlcNAc) has been shown to regulate over 3

209 eased deposition of O-linked beta-N-acetyl-d-glucosamine (O-GlcNAc) in cardiac proteins are a hallmar

210 iseases can be modified by O-linked N-acetyl-glucosamine (O-GlcNAc) in vivo.

211 beta-O-N-acetyl-D-glucosamine (O-GlcNAc) is a post-translational modificat

212 n O-GlcNAc regulation.O-linked beta-N-acetyl glucosamine (O-GlcNAc) is an important protein modificat

213 The O-linked beta-N-acetyl glucosamine (O-GlcNAc) modification dynamically regulate

214 the cell surface, the O-linked beta-N-acetyl glucosamine (O-GlcNAc) modification is a simple intracel

215 NleB functions as a translocated N-acetyl-D-glucosamine (O-GlcNAc) transferase that modifies GAPDH.

216 The effect of glucosamine on T helper cell differentiation was similar

217 ocation of a single sulfate at either C-6 of glucosamine or C-2 of uronic acid in the reducing disacc

218 be reversed by addition of excess glucose or glucosamine or exogenous HA to the culture medium.

219 manner by increasing O-GlcNAc synthesis with glucosamine or inhibiting O-GlcNAcase with thiamet-G.

220 rast, infusion of the glucokinase inhibitors glucosamine or mannoheptulose worsened glucose tolerance

221 nstrate that increasing O-GlcNAc with either glucosamine or PUGNAc improved 24-hr survival after trau

222 By comparison to the N-acetyl glucosamine parent, some of the analogues show a signifi

223 ysaccharide adhesin poly-beta-1,6-N-acetyl-D-glucosamine (PGA) by binding to the pgaABCD mRNA leader,

224 RapZ contributes to the control of glucosamine phosphate biogenesis by selectively presenti

225 Expression of HBP enzyme glucosamine-phosphate N-acetyltransferase 1 (GNPNAT1) is

226 ursors, LpxK binds almost exclusively to the glucosamine/phosphate moieties of the lipid molecule.

227 etic glycosylphosphatidylinositol analogues, glucosamine-phosphatidylinositol (glucosamine-PI) or glu

228 Glucosamine-PI caused the displacement of PrP(C) from li

229 In addition, ScGT1 cells treated with glucosamine-PI did not transmit infection following intr

230 Treatment with glucosamine-PI increased the cholesterol content of ScGT

231 We propose that treatment with glucosamine-PI modifies local micro-environments that co

232 The effect of glucosamine-PI on PrP(Sc) formation was also reversed by

233 analogues, glucosamine-phosphatidylinositol (glucosamine-PI) or glucosamine 2-O-methyl inositol octad

234 e exopolysaccharide poly-beta-1,6-N-acetyl-d-glucosamine (PNAG) by the extracellular protein IcaB is

235 e exopolysaccharide poly-beta-1,6-N-acetyl-D-glucosamine (PNAG) by the periplasmic protein PgaB is re

236 Poly-beta-1,6-N-acetyl-D-glucosamine (PNAG) is an exopolysaccharide produced by a

237 face polysaccharide poly-beta-(1-6)-N-acetyl-glucosamine (PNAG) mediates biofilm formation by some ba

238 nt deacetylation on poly-beta-1,6-N-acetyl-d-glucosamine (PNAG) oligomers, supporting previous immuno

239 A beta-(1-->6)-linked poly-N-acetyl-d-glucosamine (PNAG) surface capsule is synthesized by fou

240 s cell surface polysaccharide, poly-N-acetyl glucosamine (PNAG).

241 face polysaccharide poly-N-acetyl-beta-(1-6)-glucosamine (PNAG).

242 ntigen, a beta-(1-->6)-polymer of N-acetyl-D-glucosamine (PNAG).

243 psular polysaccharide (CP) and poly-N-acetyl glucosamine (PNAG).

244 two enzymes: uridine diphosphate-N-acetyl-D-glucosamine:polypeptidyltransferase (OGT) and O-GlcNAcas

245 ically acts on N-sulfated and 6-O-desulfated glucosamines present as monosaccharides or at the nonred

246 s on N-sulfated or N-acetylated 6-O-sulfated glucosamines present at the non-reducing end of HSGAG ol

247 a series of novel O-6 phosphate N-acetyl (d)-glucosamine prodrugs aimed at improving the oral bioavai

248 6-O-Sulfation at the glucosamine residue contributes to a wide range of biolo

249 sphosulfate to the 3-hydroxyl group of the D-glucosamine residue in an immobilized HS chain using D-g

250 The glucosamine residue of heparan sulfate can carry sulfo g

251 that would trap the 6-hydroxyl moiety of the glucosamine residue of muramic acid to generate the so-c

252 Furthermore, a preexisting N-sulfo glucosamine residue prevents the action of NDST-1 at the

253 asaccharides with 3-O-sulfo group-containing glucosamine residues at their reducing ends.

254 Enzymatic cleavage between the two N-acetyl glucosamine residues of the chitobiose core of N-glycans

255 lfation of uronic acids and 6-O-sulfation of glucosamine residues, we genetically ablated heparan sul

256 y depend on the distribution of 6-O-sulfated glucosamine residues, which is generated by glucosaminyl

257 gh detection of the NH resonances of N-sulfo-glucosamine residues.

258 ing to the product with a cluster of N-sulfo glucosamine residues.

259 at attaches beta-O-GlcNAc (beta-O-N-acetyl-D-glucosamine) residues to S. aureus WTAs.

260 complex with beta-1,6-(GlcNAc)6, GlcNAc, and glucosamine reveal a unique binding mode suitable for in

261 fter transfer of the fatty acyl group to the glucosamine ring using the thiol-specific labeling reage

262 ) and psi (psi) angles between iduronate and glucosamine rings.

263 High-dose glucosamine significantly decreased Glut1 N-glycosylatio

264 study, we developed a polymer, poly-N-acetyl-glucosamine (sNAG), with bioactive properties that may b

265 nt for the N-acetyl or N-sulfo groups on the glucosamine substrate can be explained through eliciting

266 nomer derivatives-glucosamine hydrochloride, glucosamine sulfate, galactosamine hydrochloride, and ma

267 s) GlmY and GlmZ activate the translation of glucosamine synthase (GlmS) in E. coli K-12, and in EHEC

268 saccharide is a hexaacylated disaccharide of glucosamine that is phosphorylated at the 1 and 4' posit

269 accharide is a hexa-acylated disaccharide of glucosamine that makes up the outer monolayer of the out

270 rticular the ability of fructose to generate glucosamine, the amino acid-metal complexes were heated

271 o N-phenyl carbamate (GalPUGNAc), N-acetyl-D-glucosamine-thiazoline (NGT), and N-acetyl-D-galactosami

272 pxQ in E. coli converts much of the proximal glucosamine to 2-amino-2-deoxygluconate.

273 Administration of glucosamine to GFP-LC3-transgenic mice markedly activate

274 hanced, the ability of both high glucose and glucosamine to induce insulin resistance.

275 that modifies host proteins with N-acetyl-d-glucosamine to inhibit antibacterial and inflammatory ho

276 revealed the involvement of a novel N-acetyl glucosamine transporter and an alpha/beta-fold hydrolase

277 Finally, glucosamine treatment inhibited Th1 cells in vivo, prolo

278 Glucosamine treatment of chondrocytes activated autophag

279 Glucosamine treatment, which increases UDP-GlcNAc availa

280 s in autophagy in response to starvation and glucosamine treatment.

281 A increased after O-GlcNAcylation induced by glucosamine treatments or by inhibiting O-GlcNAc transfe

282 ed step of the uridine 5'-diphospho-N-acetyl-glucosamine (UDP-GlcNAc) pathway, which provides interme

283 o occur by 4,6-dehydration of UDP-N-acetyl-d-glucosamine (UDP-GlcNAc) to UDP-2-acetamido-2,6-dideoxy-

284 e linkage between a GlcA unit and an N-sulfo glucosamine unit carrying either a 3-O-sulfo or a 6-O-su

285 eaves the linkage of a GlcA unit and N-sulfo glucosamine unit with a 2-O-sulfated GlcA residue, not a

286 fers a sulfo group to the 3-OH position of a glucosamine unit.

287 y increased N-sulfation and 6-O-sulfation of glucosamine units in response to the decrease in 2-O-sul

288 sed as the nitrogen protective group for the glucosamine units, and the addition of TMSOTf was found

289 tly regulates several chitin- and N-acetyl-D-glucosamine-utilization genes that are co-regulated duri

290 OS sialylation, increasing abundance of LA d-glucosamine versus 2,3-diamino-2,3-dideoxy-d-glucose, an

291 Glucosamine was found to be more effective for glycation

292 limit of detection of 5 nM for DABSYL-tagged glucosamine was obtained using long injections (to give

293 s, the induction of TRIB3 by high glucose or glucosamine was reversible upon removal of these substra

294 ression was also substantially stimulated by glucosamine, which bypasses GFAT, accompanied by a decre

295 fated iduronic acid linked to 6-O-sulfated N-glucosamine, which contains a free amine at position 2,

296 intramolecular anomeric protection (iMAP) of glucosamine, which facilitates concise transformation of

297 he alpha-anomeric glycoside of L-cysteinyl-D-glucosamine with L-malic acid, is a major low-molecular-

298 li lipid A is a hexaacylated disaccharide of glucosamine with secondary laurate and myristate chains

299 lent selective fluorescent responses towards glucosamine with the enhancement of fluorescence quantum

300 6-O-sulfation (6S) of glucosamine within HS chains is critical for many of the