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

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

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

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

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

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

33 3 species contained N-acetylneuraminic acid (NeuAc).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 5'-monophospho-N-acetylneuraminic acid (CMP-NeuAc) to an acceptor molecule.

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

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

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

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

71 hemical deamination of the corresponding CMP-NeuAc precursors.

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

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

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

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

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

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

78 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

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

80 ifferent than observed for solvolysis of CMP-NeuAc.

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

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

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

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

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

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

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

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

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

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

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

92 2.6 on V/K and V(max) were observed with CMP-NeuAc as the donor, and it is revealing that these isoto

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

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

95 rger than those previously measured with CMP-NeuAc.

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

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

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

99 or NeuAc, although supplementation enhanced NeuAc incorporation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 2 derivatives whose carboxyl function in the NeuAc had been modified by methyl esterification or redu

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

149 0 was measured at the terminal carbon of the NeuAc glycerol side chain.

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

151 ile parameters, and pathology as compared to NeuAc.

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

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

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

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

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

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

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

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

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

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

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

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