ライフサイエンスコーパス: asialo

1 lues, however, are drastically different for asialo (-1.37% acetonitrile units), monosialylated (-0.4

2 ate analysis of relaxin revealed an N-linked asialo, agalacto, bisected biantennary, and a core-fucos

3 were associated with species at m/z 1907.0 (asialo, agalacto, bisected, biantennary structure-NGA2B)

4 3 activity failed to transfer sialic acid to asialo alpha(1)-acid glycoprotein, indicating that this

5 ing affinities toward the acceptor substrate asialo alpha1-acid glycoprotein.

6 helial cell line, TRT-HU1) were treated with asialo-APF (as-APF), a chemically synthesized form of AP

7 homogeneous compound containing an N-linked asialo biantennary nonasaccharide glycan moiety of defin

8 The reaction product was generated using asialo-bovine submaxillary mucin as an acceptor; treatme

9 rose, affinity chromatography on immobilized asialo-bovine submaxillary mucin, and gel filtration chr

10 nting asialofetuin and the clustered Tn-rich asialo-bovine submaxillary mucin, were subsequently chos

11 The asialo capping segment has the structure: Gal-GlcNAc6S-G

12 Reconstitution of asialo cells with alpha(2,3)-specific sialyltransferase

13 ansferase was unable to restore infection in asialo cells.

14 However, clearance of asialo-pdVWF and asialo-CHO-rVWF were identical.

15 Although the particular asialo complex N-glycan isomers here were well separated

16 The asialo complex N-glycan PSD knowledge base was used to d

17 e attached bacterial glycans to homogeneous, asialo complex-type G2 N-glycans, the E. coli-derived Fc

18 ovine IgG diantennary glycopeptide (2.8 mM), asialo Cowper's gland mucin (0.06 mM), and the acrylamid

19 (transposon mutants of COH1 that express an asialo CPS or are acapsular, respectively) were grown in

20 the neutral oligosaccharides to be primarily asialo-diantennary complex-type glycans with 2, 1, or 0

21 ity and increased the membrane expression of asialo-G(M1) compared with T cells activated without IL-

22 itoyl-sn-glycero-3-phosphocholine (DPPC) and asialo-(GA1), disialo-(GD1b) and trisialo-(GT1b) ganglio

23 bolished by treatment with NK-depleting anti-asialo ganglio-N-tetraosylceramide Ab.

24 ated VEGFR2 activation, whereas the uncapped asialo-glycans favor activation of this receptor.

25 iproximin specifically bound to two types of asialo-glycans, namely to bi- and triantennary complex N

26 Thus, TLR2 in association with asialo-glycolipids presented within the context of lipid

27 cNAc beta-O-Bn (3.0 mM), fetuin triantennary asialo glycopeptide (2.4 mM), bovine IgG diantennary gly

28 b, combined with temporary inhibition of the asialo-glycoprotein receptor on hepatocytes.

29 y, we investigated whether the expression of asialo-glycoproteins (ASGPs) drives the localization and

30 e the kinetics of sialylation of a series of asialo-glycoproteins by a human sialyltransferase.

31 rate that SCID mice treated with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo dep

32 Together with asialo GM(1) and other substructures, the GM(1) methyl g

33 zation caused by anti-T cell Thy1.2 and anti-asialo GM-1 antibodies.

34 or the specificity of the antibodies for the asialo-GM(1) antigen.

35 We confirmed that asialo-GM(1) dissolved in dimethyl sulfoxide could be ad

36 Antibodies to asialo-GM(1) inhibited formation of a biofilm by P. aeru

37 These findings demonstrate that asialo-GM(1) is not a major cellular receptor for clinic

38 fresh clinical isolates of P. aeruginosa to asialo-GM(1) or the specificity of the antibodies for th

39 alo-GM(1), and adsorption of this serum with asialo-GM(1) removed antibody binding to P. aeruginosa L

40 es with commercially available antibodies to asialo-GM(1) showed that these preparations had high tit

41 Antibodies in sera raised to asialo-GM(1) were observed to bind to P. aeruginosa cell

42 es showed that adsorption of an antiserum to asialo-GM(1) with P. aeruginosa cells could remove the r

43 could remove the reactivity of antibodies to asialo-GM(1), and adsorption of this serum with asialo-G

44 Numerous studies have reported that asialo-GM(1), gangliotetraosylceramide, or moieties serv

45 ical isolates, exhibited enhanced binding to asialo-GM(1)-treated cells.

46 , similar to RMA cells or RMAS cells in anti-asialo-GM(1)-treated mice, while untransfected or ss(2)M

47 revealed specific binding only to GD1(b) and asialo-GM(1).

48 interaction is confirmed with antibodies to asialo-GM(1).

49 ely when NK cells were eliminated using anti-asialo GM1 Ab administration, but only marginally impair

50 Depletion of NK cells with anti-asialo GM1 Ab reduced or abrogated the observed antitumo

51 ouse NK cells express the surface glycolipid asialo GM1 and are implicated in the rejection of hetero

52 in diameter) in nude mice treated with anti-asialo GM1 antibodies and in severe combined immunodefic

53 immunodeficiency mice by administering anti-asialo GM1 antibodies before subcutaneous tumor injectio

54 ice, broad-spectrum oral antibiotics or anti-asialo GM1 antibodies reduce the expression of IFN-gamma

55 ntraperitoneal administration of RB6-8C5 and asialo GM1 antibodies.

56 In vivo depletion of NK cells by anti-asialo GM1 antibody abrogated the antimetastatic effects

57 e depletion of NK cells during EAM with anti-asialo GM1 antibody significantly increased myocarditis

58 We used polyclonal anti-asialo GM1 antibody to actively deplete NK cells in vivo

59 depleted of NK cells by treatment with anti-asialo GM1 antibody, and such animals did not develop TE

60 onoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant vir

61 Treatment with anti-asialo GM1 antiserum (ASGM1), which ablated circulating

62 SCID mice received rabbit anti-asialo GM1 antiserum to abrogate endogenous natural kill

63 Treatment with anti-asialo GM1 eliminated NK activity in the eye and at nono

64 emonstrate that SCID mice treated with alpha-asialo GM1 have reduction in the number of asialo GM1-ex

65 Furthermore, we provide evidence that asialo GM1 is a potentially important therapeutic target

66 mice were depleted of NK/NKT cells with anti-asialo GM1 or anti-NK1.1 Ab.

67 (NK) cell function with antibodies to either asialo GM1 or NK 1.1 reversed IL-12 inhibition of basic

68 Mice depleted of NK cells using anti-asialo GM1 showed decreased survival and higher lung bac

69 allografts by treating recipients with anti-asialo GM1 to deplete NK cells.

70 We demonstrate that asialo GM1(+) CD8(+) cells play a critical role in this

71 K-depleted (injected intravenously with anti-asialo GM1) or mock-depleted (injected intravenously wit

72 with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo depletion of endogenous NK cell

73 of IL-18 appears to be primarily mediated by asialo GM1+ cells.

74 e seen in mice treated with anti-NK1.1, anti-asialo GM1, and selected Ly49 subtype-depleted mice.

75 rtially by anti-NK1.1 and completely by anti-asialo GM1, but not by anti-CD8, Abs.

76 side series GM1, GM2, GM3, GD1A, GD1B, GT1B, asialo GM1, globotriosyl ceramide, and lactosyl ceramide

77 a-asialo GM1 have reduction in the number of asialo GM1-expressing splenocytes.

78 mice were immunodepleted of T lymphocytes or asialo GM1-positive cells, the restraint on dormant diss

79 arlier and induced lethality sooner in alpha-asialo GM1-treated animals.

80 splenic cell suspensions derived from alpha-asialo GM1-treated SCID mice show lower cytotoxicity aga

81 4.61 x 10-12 M for GM1 to 1.88 x 10-10 M for asialo GM1.

82 d with subcutaneous (s.c.) injection of anti-asialo GM1.

83 inosa type IV pili and the glycosphingolipid asialo-GM1 (aGM1) can mediate bacterial adherence to epi

84 Among these, trNK cells had reduced asialo-GM1 (AsGM1) expression relative to cNK cells, a p

85 of specific markers such as NK1.1, DX5, and asialo-GM1 (ASGM1).

86 The gangliosides GD1a, GM1, and asialo-GM1 (GA1) are natural components of murine macrop

87 enzymes transfer fucose not only to GM1 and asialo-GM1 (Gg4) but also to galactosyl globoside (Gb5)

88 ion of NK cells (via anti-IL-2Rbeta and anti-Asialo-GM1 Abs) or blockade of the NK cell activating re

89 glycoproteins (e.g. CD8) and the glycolipid asialo-GM1 also carry PNA receptors, although to a much

90 gangliosides devoid of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose

91 Unexpectedly, protection sensitive to anti-asialo-GM1 and increased NK activity were still present

92 killer cells was achieved through an IV anti-asialo-GM1 antibody injection.

93 determined by selective depletion with anti-asialo-GM1 antiserum in vivo and NK-cell-mediated cytoly

94 that it was abrogated by treatment with anti-asialo-GM1 but not anti-CD8, and was induced by CD1(-/-)

95 in gangliosides, gangliosides GM2 or GM3, or asialo-GM1 had weak inhibitory effects on alpha-synuclei

96 on the terminal galactose, but not to GM1 or asialo-GM1 in an enzyme-linked immunosorbent assay.

97 6F10 melanoma in SCID mice treated with anti-asialo-GM1 in the absence of a mononuclear infiltration,

98 Immunodepletion with anti-asialo-GM1 or anti-CD4 during C3L5-CK beta 11 vaccinatio

99 Asialo-GM1 pretreatment of MDCK monolayers likewise augm

100 anied by infiltrations of CD45+, Mac-1+, and asialo-GM1+ cells into the tumor; B220+ cells were prese

101 mature T cells, but require B, NK, and other asialo-GM1+ cells.

102 sidual host T cells, such that NK1.1+ or DX5+asialo-GM1+ T cells become the predominant T cell subset

103 d that protection afforded by NK1.1+ and DX5+asialo-GM1+ T cells derived from either donors or hosts

104 PE64Delta553pil bound specifically to asialo-GM1, and, when injected into rabbits, produced an

105 ould also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible fo

106 By contrast, complex GSLs, such as asialo-GM1, were not required for NK cell viability and

107 by treatment in vitro and in vivo with anti-asialo-GM1.

108 ence: GM1 > GM2 > GD1A > GM3 > GT1B > GD1B > asialo-GM1.

109 y), and mice depleted of NK cells using anti-asialo-GM1.

110 ely stimulate the hydrolysis of both GM2 and asialo-GM2 (GA2) by HexA and, to a lesser extent, also s

111 and of particular interest, ganglioside GM2, asialo-GM2 (GA2), and sulfatides (ST).

112 at of the oligosaccharides derived from GM2, asialo-GM2 (GalNAcbeta1-->4Galbeta1--> 4Glcbeta1-1'Cer)

113 in the fraction bound to dishes coated with asialo-GM2 (Gg3) or with anti-GM3 monoclonal antibody DH

114 era inhibited the binding of B. pertussis to asialo-GM2 and to rabbit ciliated cells.

115 nvolved in the catabolism of GM2 through the asialo-GM2 pathway.

116 The functional role of asialo-GM2+ cells was confirmed by in vivo depletion stu

117 Among the oligosaccharides derived from GM2, asialo-GM2, and 6'GM2, only the oligosaccharide from GM2

118 distributed and reduced accumulation of GM2, asialo-GM2, and bis(monoacylglycero)phosphate in brain r

119 void of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose carboxyl funct

120 recruited into PrP(Sc), whereas PrP(C) with asialo-GPIs inhibited conversion.

121 that recruiting PrP(C) with both sialo- and asialo-GPIs is a common feature of PrP(Sc) The mixtures

122 Remarkably, the proportion of sialo- versus asialo-GPIs was found to be controlled by host, tissue,

123 eature of PrP(Sc) The mixtures of sialo- and asialo-GPIs were observed in PrP(Sc) universally regardl

124 scrapie brains reported that both sialo- and asialo-GPIs were present in PrP(Sc), with the majority b

125 present in PrP(Sc), with the majority being asialo-GPIs.

126 nces for selecting PrP(C) with sialo- versus asialo-GPIs.

127 Moreover, mouse asialo-IFN-beta profoundly reduced viremia in vivo in HB

128 urthermore, the enhanced antiviral effect of asialo-IFN-beta was supported by induction of the 2'-5'

129 This modified IFN (asialo-IFN-beta) demonstrated greater inhibition of HBV

130 -cell carbohydrate, specifically recognizing asialo-lactosyl-containing carbohydrates.

131 e distribution of pI and molecular weight of asialo-, mono-, di-, tri-, and tetrasialotransferrin var

132 At high surface densities, asialo mucin mimics inhibited IAV binding to underlying

133 When capsule-deficient or asialo mutant type III strains were employed, the lectin

134 owever, unlike H1, which can bind the ligand asialo-orosomucoid (ASOR) when overexpressed in COS-7 ce

135 o-purified by affinity chromatography, using asialo-orosomucoid (ASOR)-, anti-H1-, or anti-H2-COOH-Se

136 fic receptors, but SRCL binds selectively to asialo-orosomucoid rather than generally to asialoglycop

137 function was assessed by uptake of iodinated asialo-orosomucoid, immunoglobulin (Ig) A1, and haptocor

138 ated specific uptake and degradation of 125I-asialo-orosomucoid.

139 lls with a molar ratio of 0.26 compared with asialo-orosomucoid; porcine haptocorrin bound with a mol

140 Immobilized GalNAc and asialo-ovine submaxillary mucin (rich in O-linked glycan

141 However, clearance of asialo-pdVWF and asialo-CHO-rVWF were identical.

142 In vitro, asialo-podocytes were viable, able to proliferate and di

143 mmortalized sialylation-deficient podocytes (asialo-podocytes) for functional studies.

144 gues, often through interactions with distal asialo-residues.

145 Additional asialo-triantennary and asialo-tetrantennary structures were also observed with

146 Additional asialo-triantennary and asialo-tetrantennary structures