ライフサイエンスコーパス: NeuAc

1 NeuAc alpha 2,3Gal beta 1,4 glycoconjugates may not only

2 NeuAc is present in the oligosaccharidic portion of inte

3 NeuAc-H gene expression was detected in both solid tumor

4 NeuAc-H is required for the synthesis of gangliosides co

5 ical shift dispersion due to the various 13C-NeuAc adducts on ST6Gal-I was observed in a 3D experimen

6 tes a hydrogen bond to the 4-OH of Gal in 3'-NeuAc-Le(x), forms a water-mediated hydrogen bond with t

7 binds HL-60 cells and the oligosaccharide 3'-NeuAc-Le(x).

8 uctures of K3 alone and in complexes with 3'-NeuAc-Le(x), 3'-sulfo-Le(x) and 4'-sulfo-Le(x) have been

9 for the low activity (9%) with Gal beta 1,3(NeuAc alpha 2, 6)GlcNAc beta-O-Bn, but with type 2 consi

10 the presence of the NeuAc alpha2-3Galbeta1-3(NeuAc alpha2-6)GlcNAc structural group.

11 des GT1aalpha (IV(3)NeuAc, III(6)NeuAc, II(3)NeuAc-Gg(4)OseCer) and GQ1balpha (IV(3)NeuAc, III(6)NeuA

12 c-LacCer (GM3), Gb4Cer (globoside), and Il(3)NeuAc-Gg4Cer (GM1) added exogenously to cells were incor

13 (3)H-Labeled Il(3)NeuAc-LacCer (GM3), Gb4Cer (globoside), and Il(3)NeuAc-G

14 II(3)NeuAc-Gg(4)OseCer) and GQ1balpha (IV(3)NeuAc, III(6)NeuAc, II(3)(NeuAc)(2)-Gg(4)OseCer).

15 nd the "Chol-1" gangliosides GT1aalpha (IV(3)NeuAc, III(6)NeuAc, II(3)NeuAc-Gg(4)OseCer) and GQ1balph

16 core) were tested, including GD1alpha (IV(3)NeuAc, III(6)NeuAc-Gg(4)OseCer), GD1alpha with modified

17 nd GQ1balpha (IV(3)NeuAc, III(6)NeuAc, II(3)(NeuAc)(2)-Gg(4)OseCer).

18 a1,6-fucosylation) and augmented by Asn(347) NeuAc-type sialylation (all p < 0.05).

19 Here we show that administering 3F-NeuAc to mice dramatically decreases sialylated glycans

20 lving its intracellular conversion to CMP-3F-NeuAc, a competitive inhibitor of all sialyltransferases

21 2,4,7,8,9-pentaacetyl-3Fax-Neu5Ac-CO2Me (3F-NeuAc), added to the media of cultured cells shuts down

22 After administration of 3F-NeuAc, liver enzymes in the blood are dramatically alter

23 Although blockade of sialylation with 3F-NeuAc does not affect viability of cultured cells, its u

24 g(4)OseCer) and GQ1balpha (IV(3)NeuAc, III(6)NeuAc, II(3)(NeuAc)(2)-Gg(4)OseCer).

25 1" gangliosides GT1aalpha (IV(3)NeuAc, III(6)NeuAc, II(3)NeuAc-Gg(4)OseCer) and GQ1balpha (IV(3)NeuAc

26 ested, including GD1alpha (IV(3)NeuAc, III(6)NeuAc-Gg(4)OseCer), GD1alpha with modified sialic acid r

27 4; (Hex)(5)(HexNAc)(4)(Fuc)(1) and 2100.73; (NeuAc)(1)(Hex)(5)(HexNAc)(4)(Fuc)(1), were significantly

28 e antibodies (Abs) that bind NeuAc(alpha2-8) NeuAc epitopes on GQ1b and related gangliosides are foun

29 d the terminal trisaccharide, NeuAc(alpha2-8)NeuAc(alpha2-3)Gal common to GQ1b and GD3, and conjugate

30 which react principally with NeuAc (alpha2-8)NeuAc(alpha2-3)Gal-configured disialosyl epitopes common

31 g alpha2,3-linked NeuGc but does not abolish NeuAc binding.

32 zymatically add 13C-N-acetylneuraminic acid (NeuAc or sialic acid) to glycoproteins after their prepa

33 peptides containing N-acetylneuraminic acid (NeuAc) and N-acetylhexosamine (HexNAc).

34 rms of sialic acid, N-acetylneuraminic acid (NeuAc) and N-glycolylneuraminic acid (NeuGc).

35 ans is often either N-acetylneuraminic acid (NeuAc) or N-glycolylneuraminic acid (NeuGc).

36 s, which are either N-acetylneuraminic acid (NeuAc) or N-glycolylneuraminic acid (NeuGc); the latter

37 ctive receptors for N-acetylneuraminic acid (NeuAc), the most common occurring sialic acid, in highly

38 3 species contained N-acetylneuraminic acid (NeuAc).

39 y excretion of free N-acetylneuraminic acid (NeuAc, sialic acid).

40 lipooligosaccharides containing sialic acid (NeuAc) and phosphorylcholine (PCho).

41 Sialic acid (NeuAc) is a major anion on endothelial cells (ECs) that

42 ially capped by the addition of sialic acid (NeuAc), i.e., NeuAc2 alpha-->3Gal beta1-->4GlcNAc beta1-

43 els of sialic acid (N-acetylneuraminic acid, NeuAc) in their LOS.

44 nosamine precursors of sialic acid (to alter NeuAc/NeuGc abundances) and linkage-specific sialidases

45 linkage was more abundant than alpha2-3, and NeuAc was more abundant than NeuGc.

46 The enzyme catalyzes the reaction of CTP and NeuAc to form CMP-NeuAc, which is the nucleotide sugar d

47 ycan, whereas extensions by GlcNAc, Gal, and NeuAc are favorable on the 3-arm.

48 the enzymatic hydrolysis of both GalNAc and NeuAc from GM2.

49 the enzymatic hydrolysis of both GalNAc and NeuAc from GM2.

50 scern the enzymatic hydrolyses of GalNAc and NeuAc from the GM2 epitope and established that the NeuA

51 (alpha2-3)-Gal-GlcNAc6S-Gal6S-GlcNAc6S-, and NeuAc(alpha2-3)-Gal6S-GlcNAc6S-Gal6S-GlcNAc6S- are clear

52 tructural groups such as sialyl Lewis(x) and NeuAc alpha2-3 substituted Galbeta1-4GlcNAc antennae wer

53 sed the unique cleavage product, 2,7-anhydro-NeuAc from sialoglycoconjugates.

54 specific sialidase that releases 2,7-anhydro-NeuAc instead of NeuAc from sialoglycoconjugates.

55 By using two complementary approaches (NeuAc removal by neuraminidase or its masking by NeuAc-b

56 ion of complex isobaric polar lipids such as NeuAc- and NeuGc-containing gangliosides.

57 at the masking of alpha(v)beta(3)-associated NeuAc by MAA prevents Tat/alpha(v)beta(3) interaction.

58 e that alpha2,3(O)ST is capable of attaching NeuAc to another position in C-3-substituted beta1,3Gal.

59 Anti-disialoside antibodies (Abs) that bind NeuAc(alpha2-8) NeuAc epitopes on GQ1b and related gangl

60 Most influenza A viruses bind NeuAc, but a small minority bind NeuGc.

61 c removal by neuraminidase or its masking by NeuAc-binding lectin from Maackia amurensis, MAA), we in

62 13)C-labeled N-acetylneuraminic acid ([(13)C]NeuAc) and N-glycolylneuraminic acid (NeuGc) were effici

63 ans from adult rat brain to glycans carrying NeuAc residues as their sole charged groups.

64 CMP-NeuAc produced in situ is utilized by the same enzyme to

65 CMP-NeuAc: Galbeta1,3(4)GlcNAc alpha2,3-sialyltransferase (a

66 column, and addition of synthesized 13C-CMP-NeuAc to the desialylated ST6Gal-I.

67 Sialyltransferase activities, SAT-3 (CMP-NeuAc:nLcOse4Cer alpha 2-3sialyltransferase) and SAT-4 (

68 r alpha 2-3sialyltransferase) and SAT-4 (CMP-NeuAc:GgOse4Cer alpha 2-3sialyltransferase), in Colo 205

69 acid cytidylyltransferase (EC 2.7.7.43) (CMP-NeuAc synthetase) was isolated from a Haemophilus ducrey

70 somnus with CMP-N-acetylneuraminic acid (CMP-NeuAc) or NeuAc added to the medium resulted in incorpor

71 '-monophosphate N-acetylneuraminic acid (CMP-NeuAc) synthetase.

72 5'-monophospho-N-acetylneuraminic acid (CMP-NeuAc) to an acceptor molecule.

73 sfection of the antisense vector against CMP-NeuAc: GM3 alpha2-8 sialyltransferase (GD3-synthase) gen

74 c mechanism in which CTP binds first and CMP-NeuAc dissociates last.

75 In contrast to other bacterial CMP-NeuAc synthetases, the H. ducreyi enzyme exhibited a dif

76 te following growth in medium containing CMP-NeuAc or NeuAc.

77 hemical deamination of the corresponding CMP-NeuAc precursors.

78 affinity for its sugar nucleotide donor, CMP-NeuAc, and that this catalytically inactive form of the

79 es the reaction of CTP and NeuAc to form CMP-NeuAc, which is the nucleotide sugar donor used by sialy

80 incorporation of 14C-labeled NeuAc from CMP-NeuAc into trichloroacetic acid-precipitable material wh

81 Biochemical assays indicated CMP-NeuAc:GalNAc-IgA1 alpha2,6-sialyltransferase activity in

82 sialic acid when grown in medium lacking CMP-NeuAc or NeuAc, although supplementation enhanced NeuAc

83 eaction comprising in situ production of CMP-NeuAc and sialylation of acceptor had a sharp optimum at

84 th CMP-NeuAc as well as the formation of CMP-NeuAc from 5'-CMP had a wide optimum range (pH 5.2-7.2 a

85 cat, which appears to be dissociation of CMP-NeuAc in this enzyme.

86 ifferent than observed for solvolysis of CMP-NeuAc.

87 le to another without the involvement of CMP-NeuAc.

88 Ac synthetase gene has homology to other CMP-NeuAc synthetases and to a lesser extent to CMP-2-keto-3

89 and subcellular localization of ST3GalV (CMP-NeuAc:lactosylceramide alpha2,3 sialyltransferase/GM3 sy

90 shed mutant mice that lack GM3 synthase (CMP-NeuAc:lactosylceramide alpha2,3-sialyltransferase; EC 2.

91 This enzyme synthesizes CMP-NeuAc by transferring NeuAc from the NeuAcalpha2,3Galbet

92 The derived amino acid sequence of the CMP-NeuAc synthetase gene has homology to other CMP-NeuAc sy

93 reyi pathogenesis, the gene encoding the CMP-NeuAc synthetase was cloned using degenerate oligonucleo

94 at it participates in the binding of the CMP-NeuAc, a common donor substrate for all the sialyltransf

95 he ST6-GalNAcII gene and activity of the CMP-NeuAc:GalNAc-IgA1 alpha2,6-sialyltransferase were higher

96 I, inhibited the conversion of 5'-CMP to CMP-NeuAc.

97 not inhibit the conversion of 5'-CMP to CMP-NeuAc; and (iii) the mucin core 2 compound 3-O-sulfoGalb

98 2.6 on V/K and V(max) were observed with CMP-NeuAc as the donor, and it is revealing that these isoto

99 Direct sialylation with CMP-NeuAc as well as the formation of CMP-NeuAc from 5'-CMP

100 the growth medium was supplemented with CMP-NeuAc or NeuAc, as determined by electrophoretic profile

101 rger than those previously measured with CMP-NeuAc.

102 In conclusion, NeuAc is associated with endothelial alpha(v)beta(3) and

103 osides bearing the alpha-series determinant (NeuAc alpha2,6-linked to GalNAc on a gangliotetraose cor

104 harides that terminate with the disaccharide NeuAc alpha2-3(or 6)Galbeta1.

105 or NeuAc, although supplementation enhanced NeuAc incorporation.

106 c epithelial progenitors (GEPs) that express NeuAc alpha 2,3Gal beta 1,4-glycans recognized by H. pyl

107 imulated the hydrolysis of only the external NeuAc from this ganglioside by clostridial sialidase.

108 To determine the molecular basis for NeuAc and NeuGc specificity, we performed systematic mut

109 stablished to be more powerful receptors for NeuAc than the symmetrical pyridinium- and quinolinium-b

110 n-like activity of SfaS adhesin specific for NeuAc alpha2,3-galactose; however, BMEC molecules bearin

111 of HA changed the SA binding preference from NeuAc to N-glycolylneuraminic acid (NeuGc).

112 9A, and K193R converted the specificity from NeuAc to NeuGc.

113 distinct H7 and H15 HAs can be switched from NeuAc to NeuGc binding and vice versa after the introduc

114 euAc ethyl ester, GD1a NeuAc 1-alcohol, GD1a NeuAc 1-methyl ester, GD1a NeuAc 7-alcohol, GD1a NeuAc 7

115 c 1-methyl ester, GD1a NeuAc 7-alcohol, GD1a NeuAc 7-aldehyde) on this ganglioside.

116 lic) acid residues (GD1a NeuAc 1-amide, GD1a NeuAc ethyl ester, GD1a NeuAc 1-alcohol, GD1a NeuAc 1-me

117 NeuAc 1-amide, GD1a NeuAc ethyl ester, GD1a NeuAc 1-alcohol, GD1a NeuAc 1-methyl ester, GD1a NeuAc 7

118 c 1-alcohol, GD1a NeuAc 1-methyl ester, GD1a NeuAc 7-alcohol, GD1a NeuAc 7-aldehyde) on this ganglios

119 cetylneuraminic (sialic) acid residues (GD1a NeuAc 1-amide, GD1a NeuAc ethyl ester, GD1a NeuAc 1-alco

120 NeuAc(alpha2-3)-Gal-GlcNAc6S-Gal-GlcNAc6S-, NeuAc(alpha2-3)-Gal-GlcNAc6S-Gal6S-GlcNAc6S-, and NeuAc(

121 However, NeuAc was not incorporated into the LOS of commensal iso

122 phospho-N-acetylneuraminic acid hydroxylase (NeuAc-H) and beta-1,4-N-acetylgalactosaminyl transferase

123 liosides: GQ1b alpha (IV3NeuAc,III6NeuAc,II3(NeuAc)2Gg4Cer) > GT1b = GD1a > GM3 > GM1, GD1b, and GQ1b

124 was detected by incorporation of 14C-labeled NeuAc from CMP-NeuAc into trichloroacetic acid-precipita

125 requirement for a terminal alpha2, 3-linked NeuAc and great enhancement by nearby precisely spaced a

126 Interestingly, the alpha2,3-linked NeuAc and sialyl-LewisX epitopes were only bound when pr

127 d avian H7 HAs also bound to alpha2,3-linked NeuAc and sialyl-LewisX, which have an additional fucose

128 The amount of a2,6-linked NeuAc in bovine, buffalo, goat, and donkey whey glycopro

129 -linked N-Acetylneuraminic acid (a2,6-linked NeuAc, E) was found to be the predominant sialylation ty

130 Ac(alpha)OThr) as compared with alpha-methyl-NeuAc.

131 h components substituted with four (or more) NeuAc residues, showed abundances of approximately 12, 1

132 ling approach involved removal of the native NeuAc residues from ST6Gal-I with neuraminidase, separat

133 The presence or absence of NeuAc-H gene expression in the tumor tissues and cells c

134 and was found to stimulate the hydrolysis of NeuAc from GM2 by clostridial sialidase, but not the hyd

135 d to the medium resulted in incorporation of NeuAc into the LOS.

136 e that releases 2,7-anhydro-NeuAc instead of NeuAc from sialoglycoconjugates.

137 Overproduction of NeuAc is believed to result from loss of feedback inhibi

138 ensis, MAA), we investigated the presence of NeuAc on endothelial alpha(v)beta(3) and its role in Tat

139 man tissues and the selective stimulation of NeuAc hydrolysis by GM2A protein indicate that this acti

140 id when grown in medium lacking CMP-NeuAc or NeuAc, although supplementation enhanced NeuAc incorpora

141 th medium was supplemented with CMP-NeuAc or NeuAc, as determined by electrophoretic profiles and ele

142 ing growth in medium containing CMP-NeuAc or NeuAc.

143 h CMP-N-acetylneuraminic acid (CMP-NeuAc) or NeuAc added to the medium resulted in incorporation of N

144 lic acid from CMPNeuAc generates the product NeuAc alpha2-3Gal beta1-4GlcNAc-R that is specifically b

145 hat reinvestigation of other azide-protected NeuAc donors is merited.

146 ion with glycan ligands bearing the sequence NeuAc alpha2-6Gal.

147 bisecting GlcNAc, and mono/di- sialylation (NeuAc/NeuGc).

148 ovalent inhibitors tested, 3'-sialyllactose (NeuAc alpha2-3Gal beta1-4Glc; 3'SL) was the most active

149 ive adhesin(s) that recognizes the structure NeuAc alpha2-3(or 6)Galbeta1 is arranged on the bacteria

150 or ganglioside with the following structure: NeuAc alpha 2-->3Gal beta 1-->4 GlcNAc beta 1-->3Gal bet

151 und to have the following general structure: NeuAc-(alpha 2-3/6)Gal[6SO3-](beta 1-4)GlcNAc6SO3-(beta

152 -old cartilage the three capping structures: NeuAc(alpha2-3)-Gal-GlcNAc6S-Gal-GlcNAc6S-, NeuAc(alpha2

153 SLex with internally fucosylated structures: NeuAc alpha 2-->3 Gal beta 1-->4-(Fuc alpha 1-->3) GlcNA

154 he sialyltransferase (ST3N) that synthesizes NeuAc alpha 2-3Gal linkage in asparagine-linked oligosac

155 ated structures (XX and XXI, Table 2, text): NeuAc alpha 2-->3Gal beta 1-->4GlcNAc beta 1-->3Gal beta

156 neuraminidase-treated ECs demonstrated that NeuAc is associated with both the alpha(v) and the beta(

157 Our work showed that NeuAc promotes biofilm formation, but we observed no def

158 These data suggest that NeuAc-lactose is essential for binding and that any suga

159 of GM2 activator protein, the GalNAc and the NeuAc in GM2 (GalNAcbeta1-->4(NeuAcalpha2-->3)Galbeta1--

160 The inhibitions are specific because the NeuAc-unrelated lectin from Ulex europaeus is ineffectiv

161 2 derivatives whose carboxyl function in the NeuAc had been modified by methyl esterification or redu

162 alylation as afforded by the presence of the NeuAc alpha2-3Galbeta1-3(NeuAc alpha2-6)GlcNAc structura

163 0 was measured at the terminal carbon of the NeuAc glycerol side chain.

164 rom the GM2 epitope and established that the NeuAc recognition domain of GM2 activator protein is loc

165 ile parameters, and pathology as compared to NeuAc.

166 in and Maackia amurensis lectin (specific to NeuAc alpha2,3-galactose) affinity chromatography.

167 enzyme synthesizes CMP-NeuAc by transferring NeuAc from the NeuAcalpha2,3Galbeta1,3GalNAcalpha unit o

168 thus synthesized the terminal trisaccharide, NeuAc(alpha2-8)NeuAc(alpha2-3)Gal common to GQ1b and GD3

169 x) (pK(a) values = 5.5, 9.0) and V/K(UMP)(-)(NeuAc) (pK(a)values = 6.2, 9.0).

170 A series of UMP-NeuAc radioisotopomers were prepared by chemical deamina

171 measured using mixtures of radiolabeled UMP-NeuAc's as the donor substrate and N-acetyllactosamine a

172 e novel sugar-nucleotide donor substrate UMP-NeuAc.

173 hed with use of the slow donor substrate UMP-NeuAc.

174 ion of 5'-uridine monophosphate (UMP) to UMP-NeuAc, which was found to be an inactive sialyl donor.

175 These KIEs observed using UMP-NeuAc are much larger than those previously measured wit

176 ered in 6'-sialyllactose-treated mice, while NeuAc-treated mice slowed the disease progression.

177 IgM antibodies which react principally with NeuAc (alpha2-8)NeuAc(alpha2-3)Gal-configured disialosyl