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1 , 6'-sialyllactosamine, disialyltetraose, 3'-sialyl-3-fucosyllactose, sialyllacto-N-tetraose-a, sialy
2 nation of both peripheral node addressin and sialyl 6-sulfo Lewis X in high endothelial venules, cons
4 ulfated oligosaccharide, which overlaps with sialyl 6-sulfo Lewis X, the L-selectin recognition deter
6 ant-rat model; and (v) expression of the LOS sialyl acceptor is altered in cells grown without exogen
7 ; (iv) a nanA mutant hypersialylates its LOS sialyl acceptor, corresponding to an apparent increased
8 with the 5-azido-d-glycero-d-gulo-configured sialyl adamantanylthioglycoside at -78 degrees C are sel
9 rmed that the major sialylated species has a sialyl-alpha-(2-3)-lactosyl extension off the distal hep
10 up strongly reduced the inhibitory effect of sialyl alpha2-->1 Sph on GM3-dependent adhesion, FAK, an
11 Incubation of B16 cells with 0.5-10 microM sialyl alpha2-->1 Sph or 1-5 microM lyso-GM3 reduced GM3
17 the normally cryptic core Tn (GalNAc), STn (sialyl alpha2-6 GalNAc), and TF (Gal beta1-3 GalNAc) car
18 To clarify the role of milk oligosaccharide sialyl(alpha2,3)lactose (3SL) in intestinal physiology a
21 mately 66% of the glycan pool, with alpha2-6-sialyl core 1 being the predominant O-glycan structure i
22 Of greater interest was the creation of a sialyl-di-Lewis(a)-targeting i129G1 mAb via introduction
24 -O-oxazolidinone-protected 1-adamantanylthio sialyl donor high alpha-selectivities could be achieved
27 and the performance of various picoloylated sialyl donors in glycosylations with primary glycosyl ac
29 ure of the synthetic approach was the use of sialyl donors that were protected with a C-5 trifluoroac
33 cbeta1,3Galalpha-O-Me] structures containing sialyl, fucosyl, sulfo, methyl, or fluoro substituents b
34 nalyzed the expression of sialyl Lewis X and sialyl-fucosylated core 2 O-glycan (CHO-131 antigen), re
35 effects for hydrolysis of sialyl-lactose and sialyl-galactose were 1.016 +/- 0.011 and 1.015 +/- 0.00
36 beta-dideuterium and primary 13C effects for sialyl-galactose were 1.060 +/- 0.008 and 1.032 +/- 0.00
37 trate, sialyl-lactose, and a slow substrate, sialyl-galactose, in both acid-catalyzed solvolysis and
38 bopentaose (Gb5), fucosyl-Gb5 (Globo H), and sialyl-Gb5 (SSEA4) by using overexpressed glycosyltransf
39 ,3Galbeta1,3GalNAcalpha unit of O-glycans, 3-sialyl globo unit of glycolipids, and sialylated macromo
40 ngliosides sialyl-lactotetraosylceramide and sialyl-globotetraosylceramide, and the sulfated glycosph
45 opoiesis may be regulated not by the hepatic sialyl glycoproteins, but by the ST6Gal-1 that was relea
47 dative deamination of the N-nitroso-N-acetyl sialyl glycosides leading with overall retention of conf
48 loped on the basis of the equilibration of O-sialyl hydroxylamines by reversible homolytic scission o
52 tterns range from common sialyl Lewis(x) and sialyl lacto-chains to chemically functionalized carbohy
54 demonstrated activity on both 2-3' and 2-6' sialyl lactose, while NanH demonstrated activity only on
56 rimary 13C isotope effects for hydrolysis of sialyl-lactose and sialyl-galactose were 1.016 +/- 0.011
58 effects were measured for a good substrate, sialyl-lactose, and a slow substrate, sialyl-galactose,
60 ion of hiPSC into hepatocyte-like cells, the sialyl-lactotetra epitope was rapidly down-regulated and
62 ochemistry showed distinct cell surface anti-sialyl-lactotetra staining on all seven hESC lines and t
63 id glycosphingolipids, like the gangliosides sialyl-lactotetraosylceramide and sialyl-globotetraosylc
65 unoblotting with an antibody specific to the sialyl Le(x) carbohydrate epitope detected expression on
67 acetylgalactosamine gangliosides without the sialyl-Le epitope, collectively termed, have been shown
69 ll adhesion assays, anti-Le(x), but not anti-sialyl-Le(x) monoclonal antibodies, inhibited the format
73 a mucin, isomeric oligosaccharide sequences, sialyl-Lea- and sialyl-Lex-active, could be resolved by
78 , E- and P-selectins, are thought to mediate sialyl Lewis A/X-dependent hematogenous cancer metastasi
79 P-selectin blocking monoclonal antibodies or sialyl Lewis tetrasaccharide inhibits the enhanced adher
83 pating in the synthesis of core 2-associated sialyl Lewis x (C2-O-sLe(x)), a ligand involved in selec
86 de 1) diminishes the formation of the glycan sialyl Lewis X (Neu5Acalpha2-3Galbeta1-4(Fucalpha1-3) Gl
87 E-selectin glycoprotein ligand(s); distinct sialyl Lewis X (or HECA-452 antigen)-bearing membrane pr
88 ual sulfated tetrasaccharide epitope 6-sulfo sialyl Lewis x (Siaalpha2-->3Galbeta1-->4[Fucalpha1-->3]
89 the canonical E-selectin binding determinant sialyl Lewis X (sLe(X)) and display markedly greater adh
91 emarkably, an increment of host-cell-surface sialyl Lewis X (sLe(X)) exacerbates the killing by sever
93 ligand sulfotransferase (LSST) forms 6-sulfo sialyl Lewis x (sLe(x)) on both core 2 branch and MECA-7
96 lpha1-3-fucosylated selectin ligands such as sialyl Lewis x (sLe(x)), although monoclonal antibodies
97 ty by ablating N-acetyllactosamine (LacNAc), sialyl Lewis X (sLe(X)), and related lectin ligands on e
98 hesion proteins P- and L-selectin binding to sialyl Lewis X (sLe(X))-containing ligands, and the myos
99 an intragranulocytic bacterium that utilizes sialyl Lewis x (sLe(x))-modified P-selectin glycoprotein
104 tment resulted in dose-dependent ablation of sialyl Lewis X and CHO-131 antigen expression on PSGL-1,
106 ere inhibited, we analyzed the expression of sialyl Lewis X and sialyl-fucosylated core 2 O-glycan (C
107 re colon cancer HT29 cells by using multiple Sialyl Lewis X antibodies (aSlex)-conjugated PAMAM dendr
108 ts, we propose possible pathways for 6-sulfo sialyl Lewis x biosynthesis and suggest that sulfation m
109 Pre-incubation of SSL11 with the glycan Sialyl Lewis X blocked SSL11 function and de-glycosylati
110 and glycosphingolipid structures displaying sialyl Lewis X epitopes as potential E-selectin ligands
111 ranose) action by contrasting the effects on sialyl Lewis X expression displayed by P-selectin glycop
114 nsfected cells carried comparable amounts of sialyl Lewis x in extended core 1 and core 2 branched O-
116 In a rolling assay, CHO cells expressing sialyl Lewis x in extended core 1 O-glycans supported a
118 critical function of N-glycan-linked 6-sulfo sialyl Lewis X in L-selectin-dependent lymphocyte homing
120 ied a class of N-glycans bearing the 6-sulfo sialyl Lewis X L-selectin ligand in high endothelial ven
122 at adding fucose to human Tregs, forming the Sialyl Lewis X moiety on P-selectin glycoprotein ligand-
123 to recognize both nonsulfated and 6-sulfated sialyl Lewis X on core 2 branched O-glycans, and MECA-79
124 AcT) enabled the construction of the 6-sulfo sialyl Lewis x on extended core1 O-glycans, recapitulati
126 sulfated carbohydrate structures (6-sulfated sialyl Lewis x or 6-sulfo-sLex) as a recognition determi
127 g the same sequence inhibited the binding of sialyl Lewis X or sialyl Lewis A oligosaccharides to E-s
129 n of HL-60 and B16 melanoma cells expressing sialyl Lewis X to E-selectin was also inhibited by the p
130 ied NK-92MI cells with the E-selectin ligand sialyl Lewis X to promote trafficking to bone marrow.
132 kingly, bonds between L-selectin and 6-sulfo-sialyl Lewis X were impervious to ramp rate changes.
134 and fucosylated alpha2-3 glycans (including sialyl Lewis x), both of which may be important receptor
135 rate structural analysis showed that 6-sulfo sialyl Lewis X, a dominant ligand for L-selectin, was al
137 m the neutrophil surface during rolling on a sialyl Lewis x-coated planar surface at physiological sh
138 -selectin on neutrophils during rolling on a sialyl Lewis x-coated surface that involves mechanical f
140 n the lung vasculature plays a major role in sialyl Lewis X-dependent cancer cells targeting to the l
141 n E/P-selectin doubly deficient mutant mice, sialyl Lewis X-expressing B16 melanoma cells colonized t
142 carbohydrate-dependent lung colonization of sialyl Lewis X-expressing B16-FTIII-M cells in E/P-selec
147 (MB) functionalized with the selectin ligand sialyl Lewis(a) individually (MBsLea) or dually with sLe
148 A expression) and new biomarkers (levels of sialyl Lewis(a), Lewis(x), and Aspergillus oryzae lectin
152 have reported that microspheres coated with sialyl Lewis(x) (sLe(x)) interact specifically and roll
153 -terminus of PSGL-1 through recognition of a sialyl Lewis(x) (SLe(x)) moiety linked to a properly pos
154 Binding of the P-, L-, and E-selectins to sialyl Lewis(x) (sLe(x)) retards circulating leukocytes,
155 nanometer-scale polymer construct containing sialyl Lewis(x) (sLe(x)) that is found on the surface of
156 f L-selectin and the minimal selectin ligand sialyl Lewis(x) (sLe(x)) to interact with postcapillary
157 res functionalized with the selectin ligand, sialyl Lewis(X) (sLe(X)), and an antibody against ICAM-1
158 ds are glycosylated with the tetrasaccharide sialyl Lewis(x) (sLe(x)), which contributes to bond affi
159 However, the only millimolar affinity of sialyl Lewis(x) (sLe(x)), which is the common tetrasacch
160 ted in a cell-free system; it was shown that sialyl Lewis(x) (sLe(x))-coated microspheres roll over E
161 omplex with its prime glycan target 6'-sulfo sialyl Lewis(x) A canonical motif for sialic acid recogn
163 nhibitors of selectin binding to immobilized sialyl Lewis(X) and of cell adhesion to immobilized sele
164 introduced glyco-patterns range from common sialyl Lewis(x) and sialyl lacto-chains to chemically fu
166 egulation of endothelial selectins that bind sialyl Lewis(x) ligands and activation of beta(2)-integr
168 d SIGNR7 binds preferentially to the 6-sulfo-sialyl Lewis(x) oligosaccharide, whereas SIGNR2 binds al
169 volving the binding of P- and L-selectins to sialyl Lewis(X) oligosaccharide-containing ligands.
170 Here we show that binding of E-selectin to sialyl Lewis(x) on L-selectin and PSGL-1 drives their co
171 intracellular signals elicited by binding of sialyl Lewis(X) present on salival mucins to l-selectin
174 relevant branched oligosaccharides, such as sialyl Lewis(x), as well as sulfated glycosaminoglycan-l
175 -long glass fibers, and the selectin ligand, sialyl Lewis(x), was coupled to latex microspheres.
176 nd CD11b are all required for PMN binding to sialyl Lewis(x)-bearing LS174T cells at high shear (800
178 test the hypothesis that plasma C1INH bears sialyl Lewis(x)-related moieties and therefore binds to
179 demonstrated that plasma C1INH does express sialyl Lewis(x)-related moieties on its N-glycan as dete
182 uring selectin recognition, since sLe(X) and sialyl Lewis-a (sLe(a)) were approximately 5-7-fold poor
183 in E-selectin (CD62E) to its cognate ligand, sialyl Lewis-X (sLe (X) ), displayed on circulating cell
184 binding of simple oligosaccharides based on sialyl Lewis-X (sLe(X)) and complex molecules with the c
185 amine structure (Galbeta1,4GlcNAc) to create sialyl Lewis-X (sLe(X)) and related sialofucosylated gly
186 nalysis demonstrate the presence of both the sialyl Lewis-X (sLe(X)) and the di-sialylated T-antigen
187 rks that participate in the formation of the sialyl Lewis-X (sLe(X)) epitope on O-glycans linked to a
188 r conventional Hbonds in the pentasaccharide sialyl Lewis-X (sLe(X)-5) between 5 and 37 degrees C in
189 inhibitor to reduce O-linked glycosylation, sialyl Lewis-X formation, and leukocyte adhesion via the
191 presses vertebrate motifs such as sulfo- and sialyl-Lewis A epitopes but displays a high degree of an
196 -sialylated- and alpha1,3-fucosylated-moiety sialyl-Lewis x (sLe(x)), which modifies the PSGL-1 N ter
198 ysis confirmed the expression of Lewis X and sialyl-Lewis X in the intracellular granules and on the
201 ro and in vivo because of markedly decreased sialyl-Lewis X/A carbohydrate ligand-binding epitopes on
202 pport the cooperative role of E-cadherin and sialyl-Lewis X/A-deficient MUC1 in the passive dissemina
203 sferase 5 in mice, reconstituting the glycan sialyl-Lewis(a), also known as carbohydrate antigen 19-9
204 (AFM) with cantilevers biofunctionalized by sialyl-Lewis(x) (sLe(x)) were employed to investigate Ab
205 s and displays copies of the tetrasaccharide sialyl-Lewis(x) (sLe(X)), as well as a cluster of three
206 -selectin glycoprotein ligand-1 [PSGL-1] and Sialyl-Lewis(x) [SLeX]) to rapidly target inflamed tissu
207 detect binding of the SabA adhesin domain to sialyl-Lewis(X) and Lewis(X) but not to Lewis(A), Lewis(
209 eu5Acalpha2-3Galbeta1-4GlcNAc, including the sialyl-Lewis(x) motif and structures containing 6-sulfog
210 ass spectrometric analyses revealed that the sialyl-Lewis(x) sequence [NeuAcalpha2-3Galbeta1-4(Fucalp
212 inhibited by glycoconjugates terminated with sialyl-Lewis(x) sequences or by antibodies directed agai
214 uraminic acid, 5-N-glycolyl neuraminic acid, sialyl-Lewis(X), alpha2,3-sialyl-N-acetyl-lactosamine an
215 bind tightly to sugar moieties Lewis(B) and sialyl-Lewis(X), respectively, on the surface of epithel
216 ell binding is because of markedly decreased sialyl-Lewis(x/a) (sLe(x/a)) carbohydrate ligand-binding
217 Results demonstrate that 1) the sLe(X) (sialyl-Lewis-X) epitope is expressed in P-selectin glyco
218 oll" (via interactions between selectins and sialyl-Lewis-x), and then firmly adhere to the vascular
221 ed that Ply has the highest affinity for the sialyl LewisX (sLeX) structure, with a K(d) of 1.88 x 10
222 oproteins containing active moieties such as sialyl Lewisx (sLex) with P-selectin expressed on endoth
223 terminus and by the crucial tetrasaccharide sialyl LewisX produces dramatic changes in the failure k
224 ly related to the soluble E-selectin ligand, sialyl Lewisx, and is selectively expressed in skin, lym
226 c oligosaccharide sequences, sialyl-Lea- and sialyl-Lex-active, could be resolved by HPLC as fluoresc
227 binding affinity to SNA, while alteration in sialyl linkage and terminal sialic acid structure compro
228 eptides that are mass tagged to identify the sialyl linkage, thus facilitating the analysis of these
230 erum from CRC patients, where a level of six sialyl-linkage isomers were found to be altered signific
232 and non-natural sialic acid forms, different sialyl linkages and different glycans that link to the s
233 carbohydrate motifs, allowing distinction of sialyl linkages and investigation pertaining to the effe
235 seudotype with a negatively charged sulfated sialyl lipid (NMSO3) displayed a approximately 4-fold-hi
240 l neuraminic acid, sialyl-Lewis(X), alpha2,3-sialyl-N-acetyl-lactosamine and alpha2,6-sialyl-N-acetyl
241 2,3-sialyl-N-acetyl-lactosamine and alpha2,6-sialyl-N-acetyl-lactosamine at 2.7-3.0 angstrom resoluti
242 ted in the loss of glycoforms terminating in sialyl-N-acetylhexosamine and the appearance of higher m
247 libration of 1 and mass spectral analysis of sialyl phosphates suggest that the 4O,5N-oxazolidinone a
249 dicals) poor kinetic selectivity of anomeric sialyl radicals is discussed in terms of the planar pi-t
251 ants bind a broader range of alpha2-3-linked sialyl receptor sequences of a type expressed on ciliate
254 igenic phenotype also impacted HA binding to sialyl receptors that are usually present in the human r
256 rases (polySTs) responsible for polymerizing sialyl residues from donor CMP-sialic acid are not homol
258 acid units on their surfaces, mimicking the sialyl-rich mucin layer coating epithelial cells and the
260 ta1-3[NeuAcalpha2-6]GalNAc-R), followed by 3-sialyl T antigen (NeuAcalpha2-3Galbeta1-3GalNAc-R), stru
262 n of mucin origin, with terminal fucose, the sialyl T-antigen, and N-linked oligosaccharides identifi
263 significant amounts of elaborated O-glycans (sialyl-T and disialyl-T) which were inhibited upon treat
264 mine [NeuAcalpha(2-3)Galbeta(1-4)GlcNAc] and sialyl-T antigen [NeuAcalpha(2-3)Galbeta(1-3)GalNAc], wh
269 DC with sialyl-Thomsen-Friedenreich antigen (Sialyl-T) suggests that BoNT/DC recognizes only the sial
270 lls, bearing MUC1 that predominantly carries sialyl-TF, only demonstrated an adhesive response to gal
271 Two N-acetyl 4O,5N-oxazolidinone-protected sialyl thioglycosides epimeric at the 7-position have be
273 The co-crystal structure of BoNT/DC with sialyl-Thomsen-Friedenreich antigen (Sialyl-T) suggests
274 saccharide motif alone, corresponding to the sialyl-Thomsen-Friedenreich antigen, that represents the
275 mor-associated carbohydrate antigens, Tn and sialyl Tn (STn), result from somatic mutations in the ge
276 d mucin in PanINs is an early event, whereas sialyl Tn expression is a late event in the recently def
278 on of mucin-associated carbohydrate antigen, sialyl Tn, was markedly increased only in PanlN-3 and in
279 ing protein 1) showed significant binding to sialyl-Tn (Neu5Acalpha2-6-GalNAc), a tumor marker associ
280 ed O-glycans, Tn (GalNAcalpha1-Ser/Thr), and Sialyl-Tn (Siaalpha2-6GalNAcalpha1-Ser/Thr, STn) on thei
281 ated sialylated O-glycans, the disaccharide, sialyl-Tn (sialic acid alpha2,6GalNAc), is expressed by
282 ied with immunoperoxidase staining of CD11b, sialyl-Tn (sTn) antigen (Ag), and gamma immunoglobulin (
283 and discrimination of the cancer-associated sialyl-Tn (STn) antigen was developed by using Sambucus
288 A-encoding ST6GalNAc-I and the expression of sialyl-Tn is evident, demonstrating that the expression
290 vident, demonstrating that the expression of sialyl-Tn results from switching on expression of hST6Ga
292 u5Gc incorporation into the carcinoma marker Sialyl-Tn, and is the first example of such a novel mech
295 f genes encoding proteins with homology to a sialyl transferase (cstII) and a putative N-acetylmannos
296 not exactly co-locate with the Golgi marker sialyl transferase (ST)-mRFP, nor with the t-SNAREs Memb
297 e fused the signal anchor sequences of a rat sialyl transferase and a human galactosyl transferase al
299 e natural GlcNAc, followed by sialylation by sialyl transferases gave 12 differently fucosylated and