ライフサイエンスコーパス: sLe(X

1 as conjugated to the microbubble surface (MB(sLex)).

2 s, including 6-sulfo-sialyl Lewis x (6-sulfo-sLe(x)).

3 glycan determinants such as sialyl Lewis x (sLe(x)).

4 sed O-glycan expressing sialyl Lewis x (C2-O-sLe(x)).

5 ucosylated polylactosamine (C2-O-Le(x)-Le(x)-sLe(x)).

6 sed O-glycan expressing sialyl Lewis x (C2-O-sLe(x)).

7 truct the glycan determinant sialyl Lewis x (sLex).

8 GL-1 modified by both tyrosine sulfation and SLe(X).

9 ectin and EGF (LE) domains co-complexed with SLe(X).

10 ii) generation of several glycans related to sLe(X).

11 ted HL-60 cells that are unable to construct sLe(x).

12 calcium-bound fucose of the tetrasaccharide sLe(x).

13 ctin binding at 30-100-fold lower doses than sLe(X).

14 so referred to in the literature as 6'-sulfo-sLex.

15 the sialic acid and fucose residues of C2-O-sLex.

16 Tyr-SO3 and a nearby Thr modified with C2-O-sLex.

17 o bind E-selectin 5 times more strongly than sLex.

18 man RBCs showed dose-dependent inhibition by sLeX.

19 emolytic activity and a reduced affinity for sLeX.

20 nd cell-based assays far superior to that of sLex.

21 The tetrasaccharide sialyl Lewis(x) (sLe(x)) 1 is a ligand for E-, P-, and L-selectin and, th

22 y to inhibit the binding of sialyl Lewis(x) (sLe(x), 2) bearing HL-60 cells to E-, P-, and L-selectin

23 dhesion to P-selectin in vitro, whereas free sLe(x) (5 mM) only slightly inhibits adhesion.

24 bonds in the pentasaccharide sialyl Lewis-X (sLe(X)-5) between 5 and 37 degrees C in water.

25 is of core 2-associated sialyl Lewis x (C2-O-sLe(x)), a ligand involved in selectin-mediated leukocyt

26 tested using sialyl Lewis-X oligosaccharide (sLe(x)), a natural ligand of selectin adhesion molecules

27 6-Sulfo sLe(x), a sulfated carbohydrate determinant for L-select

28 r conditions which induced expression of the sLe(x,a) epitopes increased the level of FucT-VII mRNA,

29 The addition of sLe(x/a) by either manipulation caused disadherence of t

30 The decreased sLe(x/a) fail to confer electrostatic repulsions between

31 Decreased sLe(x/a) is because of decreased alpha3/4-fucosyltransfe

32 ings support the cooperative relationship of sLe(x/a) underexpression and E-cadherin overexpression i

33 use of markedly decreased sialyl-Lewis(x/a) (sLe(x/a)) carbohydrate ligand-binding epitopes on its ov

34 n the MARY-X spheroids and increased surface sLe(x/a).

35 s of fucosyltransferase activity and surface sLe(x/a).

36 n wall shear stress within the flow chamber, sLe(X)/aICAM-1 microsphere site density, and P-selectin/

37 Our results show that sLe(X)/aICAM-1 microspheres will firmly adhere to P-sele

38 icrospheres coated with either L-selectin or sLe(x) alone showed less evidence of interaction.

39 rolling on P-selectin than beads coated with sLe(x) alone, suggesting that sulfation improves rolling

40 ted selectin ligands such as sialyl Lewis x (sLe(x)), although monoclonal antibodies (mAbs) to sLe(x)

41 mon resonance experiments determined that an sLe(X) analogue (TBC1269) competitively inhibited, via s

42 In contrast, sLex and 6-sulfo-sLex did not support any Siglec-8 bindi

43 Whereas surfaces derivatized with sLex and 6-sulfo-sLex failed to support detectable Sigle

44 ex on HEV using a panel of mAbs specific for sLex and sLex-related structures, and have examined the

45 pled independently with glycopeptide lacking sLex and with sLex lacking peptide.

46 se data indicate that high levels of surface sLex and/or related epitopes are not essential for inter

47 f staining with several mAb directed against sLex and/or sLex-related structures.

48 ethanol (AcGnG-NM) reduces the expression of sLe(X) and diminishes binding in vitro to selectin-coate

49 iver-metastatic PCa and dictate synthesis of sLe(X) and E-selectin ligands on metastatic PCa cells.

50 X-1, HECA-452, and other widely used mAbs to sLe(x) and Le(x) did not bind to WEHI-3 cells and bound

51 Dual immunohistochemical staining for sLe(x) and Le(x) expression of human colon and placental

52 try was used to detect surface expression of sLe(x) and Le(x) on CMV-infected human umbilical vein en

53 and fucosyltransferases (FT), key enzymes in sLe(x) and Le(x) synthesis, was analyzed by Northern blo

54 Finally, high levels of sLe(x) and Le(x) were expressed in CMV-infected EC in vi

55 Given the known biologic functions of sLe(x) and Le(x), we suggest that CMV induction of these

56 f membrane tethers formed by bonding between sLe(x) and p-selectin at the CEC surface, the initial me

57 Yet, regulation of sLe(X) and related E-selectin ligand expression in PCa c

58 tant role during selectin recognition, since sLe(X) and sialyl Lewis-a (sLe(a)) were approximately 5-

59 al differences in how E- and P-selectin bind SLe(X) and the molecular basis of the high-affinity inte

60 le oligosaccharides based on sialyl Lewis-X (sLe(X)) and complex molecules with the core-2 structure

61 selectin binding determinant sialyl Lewis X (sLe(X)) and display markedly greater adhesive interactio

62 Sialyl Lewis(x) (sLe(x)) and Lewis(x) (Le(x)) are known for their roles i

63 . phagocytophilum binding to sialyl Lewis x (sLe(x)) and other sialylated glycans that decorate P sel

64 (Galbeta1,4GlcNAc) to create sialyl Lewis-X (sLe(X)) and related sialofucosylated glycans on human le

65 Monomeric sialyl Lewis(X) (sLe(x)) and sLe(x)-like oligosaccharides are minimal str

66 ate the presence of both the sialyl Lewis-X (sLe(X)) and the di-sialylated T-antigen (NeuAcalpha2,3Ga

67 d with the selectin ligand, sialyl Lewis(X) (sLe(X)), and an antibody against ICAM-1, aICAM-1, are pe

68 -acetyllactosamine (LacNAc), sialyl Lewis X (sLe(X)), and related lectin ligands on effector leukocyt

69 tributions of fucose and sialic acid on C2-O-sLe(x), and the function of the peptide sequence for bin

70 Lex, sLex, and related sulfated structures are ligands for se

71 ll proportion of human blood T cells express sLeX, and their function is not fully defined.

72 Based on anti-sLe(X) antibody and lectin probing experiments on 4-F-Gl

73 sialyllactosaminyl glycans convertible into sLe(X) are abundantly expressed on human monocytes yet a

74 that L-selectin ligands that contain 6-sulfo sLe(x) are reduced at HEV.

75 2 O-glycans terminated with sialyl-Lewis x (sLe(X)) are functionally important oligosaccharides that

76 eater lung vascular binding of sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form.

77 ctures (6-sulfated sialyl Lewis x or 6-sulfo-sLex) as a recognition determinant within their heavily

78 pies of the tetrasaccharide sialyl-Lewis(x) (sLe(X)), as well as a cluster of three tyrosine sulfate

79 expression and expression of sialyl Lewisx (sLex), as defined by HECA-452 (cutaneous lymphocyte anti

80 ctive oligosaccharide moiety, sialyl Lewisx (sLex), as N-linked oligosaccharide adducts.

81 Thus, interfering with sLe(X) assembly might provide a chemotherapeutic method

82 ermediate for downstream enzymes involved in sLe(X) assembly, and (iii) generation of several glycans

83 ockdown results in reduced synthesis of C2-O-sLe(x) associated with P-selectin glycoprotein ligand-1,

84 an isomeric trisulfated GSP containing C2-O-sLe(x) at Thr-44 bound much less well.

85 2-GSP-6, which has C2-O-sLe(x) at Thr-57 and TyrSO(3) at residues 46, 48, and 51

86 lfated glycopeptide (2-GP-6) containing C2-O-sLe(x) at Thr-57 bound to P-selectin with approximately

87 that involves P-selectin-, L-selectin-, and sLe(x)-bearing ligands.

88 and have examined the function of different sLex-bearing structures using an in vitro assay of lymph

89 The results suggest that SLex biantennary and triantennary are N-linked oligosacc

90 pharmacokinetic profiles were identified for SLex biantennary and triantennary oligosaccharides but n

91 iodistribution studies established that both SLex biantennary and triantennary oligosaccharides distr

92 Simultaneous dosing of SLex biantennary or triantennary oligosaccharide with a

93 The lectin domain responsible for sLeX binding is in domain 4 of Ply, which contains candi

94 The last step in sLe(X) biosynthesis is the alpha1,3-fucosyltrasferase (F

95 - residues and a short, monofucosylated C2-O-sLe(x) bound to P-selectin with high affinity (K(d) appr

96 eads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bound to

97 PSGL-1 lacks 6-sulfo-sLex but contains sulfated tyrosine residues (Tyr-SO3)at

98 philum bound to glycopeptides that contained sLex but lacked tyrosine sulfation or a specific core-2

99 in vitro binding occurred with sCR1[desLHR-A]sLex (but not with sCR1[desLHR-A]).

100 0 A2 cell surfaces, therefore, not only lack sLe(x) but also are virtually devoid of any other sialic

101 tyrosine sulfation (GP1), and one that lacks sLe(X) but has three N-terminal tyr-SO(3) groups (SP3).

102 o sLe(X) extended from a core 2 branch (C2-O-sLe(X)), but CHO-131 demonstrated no reactivity if this

103 The reduction of sLe(X) by the 4'-deoxy analog also diminished experiment

104 e has identified the contribution of 6-sulfo sLe(x) carried on N-glycans to lymphocyte homing in mice

105 nom factor model, sCR1sLex and sCR1[desLHR-A]sLex caused substantially greater reductions in neutroph

106 MB(sLex) caused greater opacification in postischemic versu

107 functional studies, we find that human blood sLeX(+)CD4(+)T cells comprise a subpopulation expressing

108 Additionally, sLeX(+)CD4(+)T cells exclusively contain the regulatory

109 Furthermore, sLeX(+)CD8(+)T cells present a pattern of features consi

110 of 800 sites/microm(2), the rolling flux of sLe(x) coated microspheres goes through a clear maximum

111 e system; it was shown that sialyl Lewis(x) (sLe(x))-coated microspheres roll over E-selectin-coated

112 y among bacterial populations recovered from sLe(x)-competent and -deficient host cells.

113 ed by A. phagocytophilum during infection of sLe(x)-competent HL-60 cells and two HL-60 cell lines de

114 Compared to sLe(x), compound 2 showed a 30-fold improved affinity in

115 P- and L-selectin binding to sialyl Lewis X (sLe(X))-containing ligands, and the myosin-actin motor p

116 nd via L-selectin to sulfated sialyl-Lewisx (sLex)-containing carbohydrate ligands expressed on the s

117 and dynamic conditions, as did sialosyl-Lex (SLex)-containing structures in previous studies.

118 However, SLex-containing poly-LacNAc gangliosides are virtually a

119 These data suggest that sLex-decorated complement inhibitors have enhanced antii

120 sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form.

121 avasation in lung when compared with the non-sLex-decorated forms.

122 Monocytes prominently present sLe(X) decorations on an array of protein scaffolds, inc

123 eptor can be obtained through cultivation in sLe(x)-defective cell lines.

124 Despite this sLex deficiency, HL60var binds well to both E- and P-sel

125 oligosaccharide selectin antagonists inhibit sLe(x)-dependent binding with significantly enhanced pot

126 t both compounds will inhibit sialyl LewisX (sLex)-dependent cell adhesion.

127 > 3) GalNAc-ol [type 2 core with sialyl Lex (sLex) determinant].

128 In addition, we showed that sLex determinants confer L-selectin ligand activity to t

129 fucosyltransferase VI increased cell-surface sLe(x) determinants, augmented binding to fluid-phase P-

130 In contrast, sLex and 6-sulfo-sLex did not support any Siglec-8 binding at the highest

131 Together, these findings reveal that sLeX display is associated with unique functional specia

132 lycopeptides lacking either TyrSO(3) or C2-O-sLe(x) do not detectably bind.

133 10(4) and 10(5) s(-1)) for the formation of sLe(x)/E-selectin bonds.

134 ds an estimate of the reactive compliance of sLe(x)/E-selectin interactions of 0.25 A, close to that

135 The sLe(x) engineered MSCs exhibited a robust rolling respon

136 s demonstrate an almost complete loss of the sLe(X) epitope on both leukocyte N- and O-glycans.

137 inds to the sulfated sialyl Lewis x (6-sulfo-sLex) epitope present on O-glycans of various glycoprote

138 pate in the formation of the sialyl Lewis-X (sLe(X)) epitope on O-glycans linked to a leukocyte cell-

139 No adherence to Lex and sLex epitopes was detected in all the strains that were

140 crement of host-cell-surface sialyl Lewis X (sLe(X)) exacerbates the killing by several wild-type IAV

141 emonstrate that beads coated with monovalent sLe(x), exhibiting a more sparse distribution of carbohy

142 ed N-terminal peptide in human PSGL-1 and to sLex expressed on PSGL-1 or other glycoproteins.

143 Here, we demonstrate that sLe(x) expressed on human L-selectin is preferentially b

144 Among CD8(+)T cells, sLeX expression distinguishes a subset displaying low ex

145 Thus, loss of host cell sLe(x) expression coincided with both differential expre

146 sLe(x) expression on CMV-infected HUVEC was strongly up-

147 Such analysis predicts that sLe(X) expression varies directly with sialyltransferase

148 cells and two HL-60 cell lines defective for sLe(x) expression.

149 CHO-131 bound to sLe(X) extended from a core 2 branch (C2-O-sLe(X)), but

150 s surfaces derivatized with sLex and 6-sulfo-sLex failed to support detectable Siglec-8 binding, 6'-s

151 s, but a monoclonal antibody against 6-sulfo-sLe(x) fails to inhibit AmOmpA adhesion and A. marginale

152 t was hypothesized that 4-F-GlcNAc inhibited sLe(X) formation by incorporating into LacNAc and blocki

153 nal N-acetylglucosamine residue also blocked sLe(X) formation in cells.

154 3) The activity of enzymes contributing to sLe(X) formation in leukocytes likely varies as ST3[Galb

155 e acetylated form of this compound inhibited sLe(X) formation in U937 monocytic leukemia cells, sugge

156 the consequences of inhibiting FUT-mediated sLe(X) formation.

157 on the disaccharides diverts the assembly of sLe(X) from endogenous cell surface glycoconjugates.

158 archetypal CDC requires interaction with the sLeX glycolipid cellular receptor as an essential step b

159 s showed that blocking binding of Ply to the sLeX glycolipid on RBCs prevents deposition of the toxin

160 sion on P-selectin, only peptides expressing sLe(X) groups showed rolling adhesion on E-selectin.

161 P-selectin: PSGL-1-Fc > sLe(a) approximately sLe(x) > HSO(3)Le(x).

162 sCR1sLex and sCR1[desLHR-A]sLex have thus demonstrated both complement regulatory a

163 protein ligand-1 between HL60var and typical sLex(high) HL60 cells were detected.

164 Indeed, triple-transfected PSGL-1/SLeX/IL-10 MSCs transiently increased levels of IL-10 in

165 ues (Tyr-SO3)at positions 46, 48, and 51 and sLex in a core 2-based O-glycan (C2-O-sLex) on Thr at po

166 contributors to the biosynthesis of 6-sulfo sLex in the context of L-selectin ligands.

167 the effects of treatment with an analogue of SLe(x) in a chronic canine model of ischemia/reperfusion

168 ring strategy to inhibit the biosynthesis of sLe(X) in cancer cells using peracetylated 5-thio-L-fuco

169 distinct PSGL-1 peptides: one that possesses sLe(X) in conjunction with three N-terminal tyr-SO(3) gr

170 of the compounds showed better activity than sLe(x) in the P-selectin assay.

171 eu5Acalpha2-3Galbeta1-4(Fucalpha1-3) GlcNAc; sLe(X)) in tumor cells.

172 lysis of purified sCR1sLex and sCR1[desLHR-A]sLex indicated an average incorporation of 10 and 8 mol

173 sCR1[desLHR-A]sLex inhibited the binding of the monocytic cell line U9

174 Addition of sLe(x) inhibited adhesion and significantly reduced SEC

175 at microspheres coated with sialyl Lewis(x) (sLe(x)) interact specifically and roll over E-selectin a

176 s coated with combinations of L-selectin and sLe(x) interacted with surgically stimulated cremaster v

177 sLex is a carbohydrate ligand for the selectin adhesion

178 fucosylated tetrasaccharide sialyl Lewis X (sLex) is an important component of leukocyte ligands for

179 Sialyl-Lewis X (sLe(X)) is a tetrasaccharide that serves as a ligand for

180 The oligosaccharide sialyl-Lewis(x) (SLe(x)) is the probable neutrophil counterligand for end

181 ntly with glycopeptide lacking sLex and with sLex lacking peptide.

182 carry T, sialyl-T, Lewisx (Lex), sialyl Lex (sLex), lactosamine, and sialyl lactosamine determinants.

183 y ligand for E-selectin, sialyl di-Lewis(x) (sLe(x)Le(x), 1), motivated us to incorporate modificatio

184 GlcNAcbeta1-3Galbeta1-4(Fucalpha1-3)GlcNAc (sLe(x)-Le(x)-Le(x)).

185 a useful probe that can be used to modulate sLe(X) levels in cells to evaluate the consequences of i

186 The selectins bind weakly to sialyl Lewisx (SLe(X))-like glycans, but with high-affinity to specific

187 GlyCAM-1, a physiological ligand better than sLe(x)-like liposomes without additional anionic charge.

188 Monomeric sialyl Lewis(X) (sLe(x)) and sLe(x)-like oligosaccharides are minimal structures capa

189 ome surface containing a multimeric array of sLe(x)-like oligosaccharides, generates a highly potent,

190 , which displays appropriate sialyl Lewis x (sLex)-like carbohydrate determinants for L-selectin reco

191 with a subset of mAb-defined sialyl Lewis X (sLex)-like structures.

192 urface expression of a subset of mAb-defined sLex-like carbohydrates is therefore a good marker for h

193 Among the sLex-like determinants expressed by human leukocytes is

194 ude that a pool of O-glycoprotease-resistant sLex-like L-selectin ligands exist on human HEV that is

195 Although the precise molecular basis for the sLex(-/low) phenotype of HL60var remains uncertain, flow

196 untreated sections by only 30%, whereas the sLex mAb 2H5 blocks binding by approximately 60% and a c

197 We report that three sLex mAbs, 2F3, 2H5, and CSLEX-1, previously noted to bi

198 Only the anti-sLe(x) mAbs 2H5 and KM93, which also recognize nonfucosy

199 DP-fucose created many new epitopes for anti-sLe(x) mAbs such as HECA-452 and CSLEX-1.

200 Unlike anti-sLe(X) mAbs, CHO-131 binding also indicates C2GnT activi

201 We show that P-selectin's interaction with sLe(X) mechanistically facilitates firm adhesion mediate

202 We find that sLe(x) microspheres specifically interact with and roll

203 -blocking antibody or a previously described sLe(x) mimetic (CGP69669A).

204 nt synthesis (10 linear steps) of the potent sLe(x) mimetic 2.

205 A sialyl Lewis X (sLe(x)) mimetic compound, 2-(trimethylsilyl)ethyl 3-O-ca

206 These compounds represent a novel series of sLe(X) mimetics with antiinflammatory activity.

207 Sialyl Lewis X (sLex) mimetics that can function as selectin antagonists

208 ry of antagonists obtained by connecting the sLe(x) mimic to the best second-site ligand via triazole

209 ing to a second site in close proximity to a sLe(x) mimic were identified.

210 A search for noncarbohydrate sLe(x) mimics led to the development of quinic acid deri

211 ytic bacterium that utilizes sialyl Lewis x (sLe(x))-modified P-selectin glycoprotein ligand 1 as a r

212 cytophilum isolates share the ability to use sLe(x)-modified PSGL-1-dependent and -independent routes

213 rganisms of the NCH-1 strain that utilize an sLe(x)-modified PSGL-1-independent means of entry can be

214 ever, beads coated with a tyrosine-sulfated, sLe(x)-modified, PSGL-1-Fc chimera support slower rollin

215 -1 through recognition of a sialyl Lewis(x) (SLe(x)) moiety linked to a properly positioned core-2 O-

216 an average incorporation of 10 and 8 mol of sLex/mol of glycoprotein, respectively.

217 The C2-O-sLe(X) motif occurs primarily on sialomucins and has bee

218 2-based O-glycan with a sialyl Lewis x (C2-O-sLe(x)) motif at a specific Thr residue.

219 for malignant transformed cells that contain sLe(x) motifs and the neurotropism of MVMi, which is lik

220 performed after intravenous injection of MB(sLex) (n=11) or MB(CTL) (n=9) with or without prior intr

221 Notably, neither unsulfated sLex (NeuAcalpha2-3Galbeta1-4[Fucalpha1-3]GlcNAc) nor an

222 he 6-position of the GlcNAc residue (6-sulfo-sLex, NeuAcalpha2-3Galbeta1-4[Fucalpha1-3](6-O-sulfo)Glc

223 lustered array of one to four sialyl Lewisx (SLex; NeuAcalpha2-3Gal[Fucalpha1-3]beta1-4GlcNAc) determ

224 esidues and an appropriately positioned C2-O-sLex O-glycan.

225 scular binding of sCR1sLex and sCR1[desLHR-A]sLex occurred in a P-selectin-dependent manner, in contr

226 ls at immobilized concentrations of 6'-sulfo-sLex of <5 pmol/spot.

227 es directed to surface biomarkers (EpCAM and Slex) of human colorectal CTCs.

228 targeting was determined from the degree of SLex oligosaccharide targeting relative to a sialyl olig

229 trols, whereas monovalent and tetraantennary SLex oligosaccharides failed to mediate specific kidney

230 es but not for monovalent and tetraantennary SLex oligosaccharides or sialyl oligosaccharide controls

231 he N terminus of human PSGL-1 that presented sLex on an O-glycan.

232 cells expressing PSGL-1 in cooperation with sLex on both N-and O-glycans.

233 Priming inhibited expression of sLex on cell surface glycoconjugates, which reduced E-se

234 d differentially to O-linked versus N-linked sLex on glycoproteins.

235 and rolling is dependent on Tyr-SO3 and C2-O-sLex on GSP-6.

236 We have examined the expression of sLex on HEV using a panel of mAbs specific for sLex and

237 ulfation or a specific core-2 orientation of sLex on the O-glycan.

238 tide to GSP-6, termed GSP-6', which contains sLe(x) on an extended core 1-based O-glycan, does not bi

239 a result of significantly decreased 6-sulfo sLe(x) on HEV L-selectin counterreceptors, relative to L

240 tennary N-glycans, and 3) reduced LacNAc and sLe(X) on N-glycans and on core 2 O-glycans.

241 51 and sLex in a core 2-based O-glycan (C2-O-sLex) on Thr at position 57.

242 sferase (LSST) forms 6-sulfo sialyl Lewis x (sLe(x)) on both core 2 branch and MECA-79-positive exten

243 Sialyl Lewis X (sLe(X)) on prostate cancer (PCa) cells is thought to pro

244 Clustered presentation of sialyl Lewis X (sLe(X)) on tumor cell mucins is thought to facilitate me

245 )), although monoclonal antibodies (mAbs) to sLe(x) or Le(x) reportedly do not bind to murine leukocy

246 sulfation did not mask epitopes for mAbs to sLe(x) or Le(x).

247 4 minutes after intravenous injection of MB(sLex) or MB(CTL).

248 er difucosylated polylactosamine (C2-O-Le(x)-sLe(x)) or trifucosylated polylactosamine (C2-O-Le(x)-Le

249 f aICAM-1/ICAM-1 interaction is greater when sLe(X)/P-selectin interactions are present.

250 Separately, sLe(X)/P-selectin interactions support rolling and aICAM

251 the IgG immune complex model, sCR1[desLHR-A]sLex possessed greater protective effects relative to sC

252 -5T-Fuc, that blocks FUT activity and limits sLe(X) presentation on HepG2 cells with an EC(50) in the

253 Selectins bind to sialylated and fucosylated sLe(x) receptors, and two enzymes, fucosyltransferase IV

254 Sialyl Lewis X (sLeX) regulates T cell trafficking from the vasculature

255 higher in cultured T lymphoblasts expressing sLe(x)-related epitopes and both selectin ligands than i

256 r in conjunction with E-selectin ligands and sLe(x)-related epitopes on human T cells.

257 ds and sialylated Lewis(x)-related epitopes (sLe(x)-related epitopes) in human T lymphoblasts.

258 inguished by the mAb HECA-452, which detects sLe(X)-related glycans.

259 using a panel of mAbs specific for sLex and sLex-related structures, and have examined the function

260 ith several mAb directed against sLex and/or sLex-related structures.

261 ual TyrSO(3) residues, the placement of C2-O-sLe(x) relative to TyrSO(3), the relative contributions

262 teins, designated sCR1sLex and sCR1[desLHR-A]sLex, respectively, retained the complement regulatory a

263 and catch-bond formation with L-selectin via sLe(x), resulting in focal clusters that deliver a disti

264 P-, L-, and E-selectins to sialyl Lewis(x) (sLe(x)) retards circulating leukocytes, thereby facilita

265 lycosyltransferases that regulate display of sLe(X) reveal high transcript levels among circulating m

266 Similar binding kinetics are expected for sLe(X)-selectin interactions.

267 tins with low affinity comparable to that of sLe(X)-selectin interactions.

268 with sulfated derivatives of sialyl Lewis x [sLe(x): Sia alpha 2-->3Gal beta 1-->4(Fuc alpha 1-->3)Gl

269 Results demonstrate that 1) the sLe(X) (sialyl-Lewis-X) epitope is expressed in P-select

270 coated with the saccharides sialyl Lewis(x) (sLe(x)), sialyl Lewis(a) (sLe(a)), and sulfated Lewis(x)

271 de that Siglec-8 binds preferentially to the sLex structure bearing an additional sulfate ester on th

272 liosides from groups i and ii above, lacking SLex structure, are the major membrane components of leu

273 the highest affinity for the sialyl LewisX (sLeX) structure, with a K(d) of 1.88 x 10(-5) M.

274 fation on two tyrosine residues and O-linked sLex structures that are presented within its highly aci

275 tin ligand expression and related LacNAc and sLe(X) structures, MALDI-TOF and MALDI-TOF/TOF mass spec

276 ydrates, we found that CL40 bound to 6-sulfo sLe(x) structures, on both core 2 and extended core 1 st

277 upport detectable Siglec-8 binding, 6'-sulfo-sLex supported significant binding with a Kd of 2.3 micr

278 the assembly of oligosaccharides related to sLe(X) synthesis, and the assembly of oligosaccharides o

279 ycans released from 4-F-GlcNAc-treated human sLe(X) (+) T cells and leukemic KG1a cells.

280 sible the biosynthesis of the sialyl-Lewisx (sLex) tetrasaccharide (NeuNAcalpha2-3Galbeta1-4(Fucalpha

281 olymer construct containing sialyl Lewis(x) (sLe(x)) that is found on the surface of leukocytes and m

282 shed detectable binding of the residual C2-O-sLe(x)-Thr to P-selectin, demonstrating that the peptide

283 There was greater adhesion of MB(sLex) to inflamed versus noninflamed endothelium (P = 0.

284 the minimal selectin ligand sialyl Lewis(x) (sLe(x)) to interact with postcapillary venules in the ab

285 e-sulfated, in addition to glycosylated with sLe(X), to successfully interact with P-selectin.

286 otein ligand-1 [PSGL-1] and Sialyl-Lewis(x) [SLeX]) to rapidly target inflamed tissues and that expre

287 Although all peptides expressing sLe(X), tyr-SO(3), or both supported some form of rollin

288 y of the interactions between L-selectin and sLe(x) under flow.

289 bind with high affinity to glycolipid-linked sLex, vary in their ability to stain HEV in different ly

290 idues and a core 1-based O-glycan expressing sLex was reduced by approximately 90%.

291 if this oligosaccharide lacked fucose or if sLe(X) was extended from a core 1 branch.

292 levers biofunctionalized by sialyl-Lewis(x) (sLe(x)) were employed to investigate Abeta-altered mecha

293 odified proteins, sCR1sLex and sCR1[desLHR-A]sLex, were assessed in the L-selectin- and P-selectin-de

294 ed with the tetrasaccharide sialyl Lewis(x) (sLe(x)), which contributes to bond affinity and specific

295 only millimolar affinity of sialyl Lewis(x) (sLe(x)), which is the common tetrasaccharide epitope of

296 alpha1,3-fucosylated-moiety sialyl-Lewis x (sLe(x)), which modifies the PSGL-1 N terminus, is import

297 roxyl group of the alpha1-3-linked fucose of sLe(X), which may account for the enhanced host cell kil

298 or their ability to block the interaction of sLex with P-selectin.

299 ining active moieties such as sialyl Lewisx (sLex) with P-selectin expressed on endothelial cells.

300 tyr-SO(3) groups (SGP3), one that possesses sLe(X) without tyrosine sulfation (GP1), and one that la