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1 ate analysis of relaxin revealed an N-linked asialo, agalacto, bisected biantennary, and a core-fucos
2 3 activity failed to transfer sialic acid to asialo alpha(1)-acid glycoprotein, indicating that this
3 ing affinities toward the acceptor substrate asialo alpha1-acid glycoprotein.
4 helial cell line, TRT-HU1) were treated with asialo-APF (as-APF), a chemically synthesized form of AP
5  homogeneous compound containing an N-linked asialo biantennary nonasaccharide glycan moiety of defin
6     The reaction product was generated using asialo-bovine submaxillary mucin as an acceptor; treatme
7 rose, affinity chromatography on immobilized asialo-bovine submaxillary mucin, and gel filtration chr
8 nting asialofetuin and the clustered Tn-rich asialo-bovine submaxillary mucin, were subsequently chos
9                                          The asialo capping segment has the structure: Gal-GlcNAc6S-G
10                            Reconstitution of asialo cells with alpha(2,3)-specific sialyltransferase
11 ansferase was unable to restore infection in asialo cells.
12                      Although the particular asialo complex N-glycan isomers here were well separated
13                                          The asialo complex N-glycan PSD knowledge base was used to d
14 ovine IgG diantennary glycopeptide (2.8 mM), asialo Cowper's gland mucin (0.06 mM), and the acrylamid
15  (transposon mutants of COH1 that express an asialo CPS or are acapsular, respectively) were grown in
16 the neutral oligosaccharides to be primarily asialo-diantennary complex-type glycans with 2, 1, or 0
17 ity and increased the membrane expression of asialo-G(M1) compared with T cells activated without IL-
18 itoyl-sn-glycero-3-phosphocholine (DPPC) and asialo-(GA1), disialo-(GD1b) and trisialo-(GT1b) ganglio
19 bolished by treatment with NK-depleting anti-asialo ganglio-N-tetraosylceramide Ab.
20 iproximin specifically bound to two types of asialo-glycans, namely to bi- and triantennary complex N
21               Thus, TLR2 in association with asialo-glycolipids presented within the context of lipid
22 cNAc beta-O-Bn (3.0 mM), fetuin triantennary asialo glycopeptide (2.4 mM), bovine IgG diantennary gly
23 b, combined with temporary inhibition of the asialo-glycoprotein receptor on hepatocytes.
24 rate that SCID mice treated with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo dep
25                                Together with asialo GM(1) and other substructures, the GM(1) methyl g
26 zation caused by anti-T cell Thy1.2 and anti-asialo GM-1 antibodies.
27 or the specificity of the antibodies for the asialo-GM(1) antigen.
28                            We confirmed that asialo-GM(1) dissolved in dimethyl sulfoxide could be ad
29                                Antibodies to asialo-GM(1) inhibited formation of a biofilm by P. aeru
30              These findings demonstrate that asialo-GM(1) is not a major cellular receptor for clinic
31  fresh clinical isolates of P. aeruginosa to asialo-GM(1) or the specificity of the antibodies for th
32 alo-GM(1), and adsorption of this serum with asialo-GM(1) removed antibody binding to P. aeruginosa L
33 es with commercially available antibodies to asialo-GM(1) showed that these preparations had high tit
34                 Antibodies in sera raised to asialo-GM(1) were observed to bind to P. aeruginosa cell
35 es showed that adsorption of an antiserum to asialo-GM(1) with P. aeruginosa cells could remove the r
36 could remove the reactivity of antibodies to asialo-GM(1), and adsorption of this serum with asialo-G
37          Numerous studies have reported that asialo-GM(1), gangliotetraosylceramide, or moieties serv
38 ical isolates, exhibited enhanced binding to asialo-GM(1)-treated cells.
39 , similar to RMA cells or RMAS cells in anti-asialo-GM(1)-treated mice, while untransfected or ss(2)M
40 revealed specific binding only to GD1(b) and asialo-GM(1).
41  interaction is confirmed with antibodies to asialo-GM(1).
42 ely when NK cells were eliminated using anti-asialo GM1 Ab administration, but only marginally impair
43              Depletion of NK cells with anti-asialo GM1 Ab reduced or abrogated the observed antitumo
44 ouse NK cells express the surface glycolipid asialo GM1 and are implicated in the rejection of hetero
45  in diameter) in nude mice treated with anti-asialo GM1 antibodies and in severe combined immunodefic
46  immunodeficiency mice by administering anti-asialo GM1 antibodies before subcutaneous tumor injectio
47 ice, broad-spectrum oral antibiotics or anti-asialo GM1 antibodies reduce the expression of IFN-gamma
48 ntraperitoneal administration of RB6-8C5 and asialo GM1 antibodies.
49        In vivo depletion of NK cells by anti-asialo GM1 antibody abrogated the antimetastatic effects
50 e depletion of NK cells during EAM with anti-asialo GM1 antibody significantly increased myocarditis
51                      We used polyclonal anti-asialo GM1 antibody to actively deplete NK cells in vivo
52  depleted of NK cells by treatment with anti-asialo GM1 antibody, and such animals did not develop TE
53 onoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant vir
54                          Treatment with anti-asialo GM1 antiserum (ASGM1), which ablated circulating
55               SCID mice received rabbit anti-asialo GM1 antiserum to abrogate endogenous natural kill
56                          Treatment with anti-asialo GM1 eliminated NK activity in the eye and at nono
57 emonstrate that SCID mice treated with alpha-asialo GM1 have reduction in the number of asialo GM1-ex
58        Furthermore, we provide evidence that asialo GM1 is a potentially important therapeutic target
59 mice were depleted of NK/NKT cells with anti-asialo GM1 or anti-NK1.1 Ab.
60 (NK) cell function with antibodies to either asialo GM1 or NK 1.1 reversed IL-12 inhibition of basic
61         Mice depleted of NK cells using anti-asialo GM1 showed decreased survival and higher lung bac
62  allografts by treating recipients with anti-asialo GM1 to deplete NK cells.
63                          We demonstrate that asialo GM1(+) CD8(+) cells play a critical role in this
64 K-depleted (injected intravenously with anti-asialo GM1) or mock-depleted (injected intravenously wit
65 with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo depletion of endogenous NK cell
66 of IL-18 appears to be primarily mediated by asialo GM1+ cells.
67 e seen in mice treated with anti-NK1.1, anti-asialo GM1, and selected Ly49 subtype-depleted mice.
68 rtially by anti-NK1.1 and completely by anti-asialo GM1, but not by anti-CD8, Abs.
69 side series GM1, GM2, GM3, GD1A, GD1B, GT1B, asialo GM1, globotriosyl ceramide, and lactosyl ceramide
70 a-asialo GM1 have reduction in the number of asialo GM1-expressing splenocytes.
71 mice were immunodepleted of T lymphocytes or asialo GM1-positive cells, the restraint on dormant diss
72 arlier and induced lethality sooner in alpha-asialo GM1-treated animals.
73  splenic cell suspensions derived from alpha-asialo GM1-treated SCID mice show lower cytotoxicity aga
74 4.61 x 10-12 M for GM1 to 1.88 x 10-10 M for asialo GM1.
75 d with subcutaneous (s.c.) injection of anti-asialo GM1.
76 inosa type IV pili and the glycosphingolipid asialo-GM1 (aGM1) can mediate bacterial adherence to epi
77          Among these, trNK cells had reduced asialo-GM1 (AsGM1) expression relative to cNK cells, a p
78  of specific markers such as NK1.1, DX5, and asialo-GM1 (ASGM1).
79              The gangliosides GD1a, GM1, and asialo-GM1 (GA1) are natural components of murine macrop
80  enzymes transfer fucose not only to GM1 and asialo-GM1 (Gg4) but also to galactosyl globoside (Gb5)
81  glycoproteins (e.g. CD8) and the glycolipid asialo-GM1 also carry PNA receptors, although to a much
82 gangliosides devoid of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose
83   Unexpectedly, protection sensitive to anti-asialo-GM1 and increased NK activity were still present
84 killer cells was achieved through an IV anti-asialo-GM1 antibody injection.
85  determined by selective depletion with anti-asialo-GM1 antiserum in vivo and NK-cell-mediated cytoly
86 that it was abrogated by treatment with anti-asialo-GM1 but not anti-CD8, and was induced by CD1(-/-)
87 in gangliosides, gangliosides GM2 or GM3, or asialo-GM1 had weak inhibitory effects on alpha-synuclei
88 on the terminal galactose, but not to GM1 or asialo-GM1 in an enzyme-linked immunosorbent assay.
89 6F10 melanoma in SCID mice treated with anti-asialo-GM1 in the absence of a mononuclear infiltration,
90                    Immunodepletion with anti-asialo-GM1 or anti-CD4 during C3L5-CK beta 11 vaccinatio
91                                              Asialo-GM1 pretreatment of MDCK monolayers likewise augm
92 anied by infiltrations of CD45+, Mac-1+, and asialo-GM1+ cells into the tumor; B220+ cells were prese
93 mature T cells, but require B, NK, and other asialo-GM1+ cells.
94 sidual host T cells, such that NK1.1+ or DX5+asialo-GM1+ T cells become the predominant T cell subset
95 d that protection afforded by NK1.1+ and DX5+asialo-GM1+ T cells derived from either donors or hosts
96        PE64Delta553pil bound specifically to asialo-GM1, and, when injected into rabbits, produced an
97 ould also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible fo
98 ence: GM1 > GM2 > GD1A > GM3 > GT1B > GD1B > asialo-GM1.
99 y), and mice depleted of NK cells using anti-asialo-GM1.
100  by treatment in vitro and in vivo with anti-asialo-GM1.
101 ely stimulate the hydrolysis of both GM2 and asialo-GM2 (GA2) by HexA and, to a lesser extent, also s
102 and of particular interest, ganglioside GM2, asialo-GM2 (GA2), and sulfatides (ST).
103 at of the oligosaccharides derived from GM2, asialo-GM2 (GalNAcbeta1-->4Galbeta1--> 4Glcbeta1-1'Cer)
104  in the fraction bound to dishes coated with asialo-GM2 (Gg3) or with anti-GM3 monoclonal antibody DH
105 era inhibited the binding of B. pertussis to asialo-GM2 and to rabbit ciliated cells.
106 nvolved in the catabolism of GM2 through the asialo-GM2 pathway.
107                       The functional role of asialo-GM2+ cells was confirmed by in vivo depletion stu
108 Among the oligosaccharides derived from GM2, asialo-GM2, and 6'GM2, only the oligosaccharide from GM2
109 distributed and reduced accumulation of GM2, asialo-GM2, and bis(monoacylglycero)phosphate in brain r
110 void of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose carboxyl funct
111  recruited into PrP(Sc), whereas PrP(C) with asialo-GPIs inhibited conversion.
112  that recruiting PrP(C) with both sialo- and asialo-GPIs is a common feature of PrP(Sc) The mixtures
113  Remarkably, the proportion of sialo- versus asialo-GPIs was found to be controlled by host, tissue,
114 eature of PrP(Sc) The mixtures of sialo- and asialo-GPIs were observed in PrP(Sc) universally regardl
115 scrapie brains reported that both sialo- and asialo-GPIs were present in PrP(Sc), with the majority b
116 nces for selecting PrP(C) with sialo- versus asialo-GPIs.
117  present in PrP(Sc), with the majority being asialo-GPIs.
118                              Moreover, mouse asialo-IFN-beta profoundly reduced viremia in vivo in HB
119 urthermore, the enhanced antiviral effect of asialo-IFN-beta was supported by induction of the 2'-5'
120                           This modified IFN (asialo-IFN-beta) demonstrated greater inhibition of HBV
121 -cell carbohydrate, specifically recognizing asialo-lactosyl-containing carbohydrates.
122 e distribution of pI and molecular weight of asialo-, mono-, di-, tri-, and tetrasialotransferrin var
123                    When capsule-deficient or asialo mutant type III strains were employed, the lectin
124 owever, unlike H1, which can bind the ligand asialo-orosomucoid (ASOR) when overexpressed in COS-7 ce
125 o-purified by affinity chromatography, using asialo-orosomucoid (ASOR)-, anti-H1-, or anti-H2-COOH-Se
126 fic receptors, but SRCL binds selectively to asialo-orosomucoid rather than generally to asialoglycop
127 function was assessed by uptake of iodinated asialo-orosomucoid, immunoglobulin (Ig) A1, and haptocor
128 ated specific uptake and degradation of 125I-asialo-orosomucoid.
129 lls with a molar ratio of 0.26 compared with asialo-orosomucoid; porcine haptocorrin bound with a mol
130                       Immobilized GalNAc and asialo-ovine submaxillary mucin (rich in O-linked glycan
131 gues, often through interactions with distal asialo-residues.
132           Additional asialo-triantennary and asialo-tetrantennary structures were also observed with
133                                   Additional asialo-triantennary and asialo-tetrantennary structures

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