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1  Gal(beta1-4)GlcNac(beta1-3)Gal(beta1-4)Glc (lacto-N-neotetraose).
2  with both UDP:Mg(2+) and a glycan acceptor, lacto-N-neotetraose.
3  were much lower than the strains expressing lacto-N-neotetraose.
4 that recognizes the terminal disaccharide of lacto-N-neotetraose.
5              In contrast, replacement of the lacto-N-neotetraose alpha-chain (Galbeta1-4GlcNAcbeta1-3
6 major structural differences are seen in the lacto-N-neotetraose alpha-chain.
7        Strain F62 (Opa-Pil+), expressing the lacto-N-neotetraose and the galNac-lacto-N-neotetraose L
8 b even when the glycose chain from HepI bore lacto-N-neotetraose at the terminus.
9 ons; a trend toward higher concentrations of lacto-N-neotetraose being associated with reduced transm
10  against RBCs can be blocked with the glycan lacto-N-neotetraose by inhibiting binding to the cell su
11 tor (ASGP-R) and the terminal lactosamine of lacto-N-neotetraose-expressing gonococcal lipooligosacch
12 s administered daily with or without the HMO lacto-N-neotetraose for 28 days.
13 ominantly ester C4b-LOS bonds were seen when lacto-N-neotetraose formed the terminus of the glycose c
14 trated that F62, but not the strains lacking lacto-N-neotetraose, formed extensive and intimate assoc
15 ed ions consistent with known LOS which have lacto-N-neotetraose (Galbeta1-->4GlcNAcbeta1-->3Galbeta1
16               Inhibition studies showed that lacto-N-neotetraose (Galbeta1-4GlcNAcbeta1-3Galbeta1-4Gl
17 dies (mAbs) 1B2(+) and 06B4(+)) and GalNAc-->lacto-N-neotetraose (gangliosyl; mAb 1-1-M+) oligosaccha
18 sult indicated that the inability to add the lacto-N-neotetraose group to the 559 LOS is not due to a
19 LOS produced by mutant 559 revealed that the lacto-N-neotetraose group which is attached to heptose I
20 dherence of F62, but not the strains lacking lacto-N-neotetraose, induced the rearrangement of actin
21  An antigen that is dependent on the glycose lacto-N-neotetraose induces IgG in humans that is bacter
22 failed to bind to immobilized sialic acid or lacto-N-neotetraose, known pneumococcal ligands on eukar
23  were observed for the abundant, neutral HMO lacto-N-neotetraose (LNnT) [RD -0.273 (95% confidence in
24 ce of bacteria to epithelial cells in vitro--lacto-N-neotetraose (LNnT) and its alpha2-3- and alpha2-
25 erogroup C meningococcal strains bearing the lacto-N-neotetraose (LNnT) structure on lipooligosacchar
26 (HMO), such as 2'-fucosyllactose (2'-FL) and lacto-N-neotetraose (LNnT), enhance iron absorption in i
27  the combination of higher concentrations of lacto-N-neotetraose (LNnT), lacto-N-tetraose (LNT), lact
28 he lipooligosaccharide sialic acid acceptor, lacto-N-neotetraose (LNnT), of nine meningococcal strain
29 inth parasites, lacto-N-fucopentaose III and lacto-N-neotetraose (LNnT).
30 topes consisting of both core structures and lacto-N-neotetraose (LNnT).
31                             The sialylatable lacto-N-neotetraose (LNnT; Gal-GlcNAc-Gal-Glc) moiety fr
32  and Neisseria meningitidis both express the lacto-N-neotetraose (LNT) lipooligosaccharide (LOS) mole
33 ely; the other (termed 398079) expressed the lacto-N-neotetraose (LNT; Galbeta1 --> 4GlcNAcbeta1 -->
34  isogenic derivative that expressed only the lacto-N-neotetraose LOS (F62 Delta lgtD), adhered to, an
35                                              Lacto-N-neotetraose LOS capped with Kdn and Kdn7N(3) bou
36 n the absence of detectable Opa protein, the lacto-N-neotetraose LOS promotes gonococcal invasion int
37 ssing the lacto-N-neotetraose and the galNac-lacto-N-neotetraose LOS, and its isogenic derivative tha
38 e terminal Galbeta1-->4GlcNAc epitope in the lacto-N-neotetraose moiety of the wild-type LOS structur
39                        These strains share a lacto-N-neotetraose (nLc4) LOS alpha chain.
40 ed no binding to its nonfucosylated homolog, lacto-N-neotetraose, or to oligosaccharides present on k
41 rains that express LOS molecules lacking the lacto-N-neotetraose structure were similar to that seen
42 tudies indicated that an interaction between lacto-N-neotetraose-terminal LOS and ASGP-R allows gonoc
43 a unique immune evasion strategy wherein the lacto-N-neotetraose termini of lipooligosaccharide (LOS)
44 1Hep2KDO2lipid A but without the addition of lacto-N-neotetraose to HepI or glucose to HepII.
45 ease in fucosyl-disialyl-lacto-N-hexaose and lacto-N-neotetraose was associated with 0.04% higher (P