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1 ctures with increased branching and extended poly-N-acetyllactosamine.
2 beta1-3GalNAc termini, and some increases in poly-N-acetyllactosamines.
3 in adding a galactose to linear and branched poly-N-acetyllactosamines.
4 fficiently add N-acetyllactosamine to linear poly-N-acetyllactosamines.
5 onstrated that itraconazole globally reduced poly-N-acetyllactosamine and tetra-antennary complex N-g
7 nsferases, which play important roles in how poly-N-acetyllactosamines are synthesized in different a
9 found that 4-F-GlcNAc (putative inhibitor of poly-N-acetyllactosamine biosynthesis) was more potent t
11 bodies with IGHV4-34*01 heavy chains bind to poly-N-acetyllactosamine carbohydrates (I/i antigen) on
12 mannosyl core may carry predominantly linear poly-N-acetyllactosamine chains, whereas the Manalpha1-3
16 that TbGT8 influences the processing of the poly N-acetyllactosamine-containing asparagine-linked gl
18 on T cells, indicating direct inhibition on poly-N-acetyllactosamine elongation and selectin-binding
20 poly-N-acetyllactosamine synthesis, allowing poly-N-acetyllactosamine extension mostly along the line
22 the branched acceptor than the summation of poly-N-acetyllactosamines formed individually on each un
23 inyltransferase, was capable of synthesizing poly-N-acetyllactosamine in core 2 branched oligosacchar
24 irely consistent with previous findings that poly-N-acetyllactosamines in human erythrocytes, PA-1 em
26 In the present study, we first found that poly-N-acetyllactosamines in N-glycans are most efficien
27 in the presence of core 1 O-glycans, but not poly-N-acetyllactosamine, in apically targeted MUC1 and
33 tosamine (LN; Galbeta1-4GlcNAc) sequences on poly-N-acetyllactosamine (PL; (-3Galbeta1-4GlcNAcbeta1-)
34 sed in olfactory sensory neurons (OSNs) with poly-N-acetyllactosamine (PLN) oligosaccharides determin
35 in exhibited higher binding for glycans with poly-N-acetyllactosamine (poly(LacNAc)) sequences (Galbe
37 essing moderate amounts of sialyl Lewis X in poly-N-acetyllactosamines produced large numbers of lung
38 a paucity of the Lewis(x) sequence based on poly-N-acetyllactosamine recognized by anti-SSEA-1; (ii)
39 n of N-acetylglucosamine residues within the poly(N-acetyllactosamine) repeat sequence and signals re
40 que LOS glycoforms containing di-, tri-, and poly-N-acetyllactosamine repeats added to the terminal r
41 n of branched oligosaccharides with multiple poly-N-acetyllactosamine repeats is nearly abolished by
44 ever, they produced extended GlcNAc-sulfated poly-N-acetyllactosamine structures with more than four
45 to longer carbohydrate substrates that have poly-N-acetyllactosamine structures, suggesting the invo
46 ndicate that beta4Gal-TIV is responsible for poly-N-acetyllactosamine synthesis in core 2 branched O-
47 These results, taken together, indicate that poly-N-acetyllactosamine synthesis in N-glycans and core
49 branch is a rate-limiting step in I-branched poly-N-acetyllactosamine synthesis, allowing poly-N-acet
50 B3GNT1, an enzyme proposed to be involved in poly-N-acetyllactosamine synthesis, were causal for cong
51 To determine how this increased synthesis of poly-N-acetyllactosamines takes place, the branched acce
52 on at multiple internal GlcNAc of unbranched poly-N-acetyllactosamine, termed "myeloglycan," the phys
53 branched O-glycans contain fewer and shorter poly-N-acetyllactosamines than N-glycans in many cells.
54 tylglucosaminyltransferase, the formation of poly-N-acetyllactosamine was found to be extremely ineff
57 rgeting when galectin-3, with preference for poly-N-acetyllactosamine, was depleted from polarized MD
58 cetyllactosamine branches attached to linear poly-N-acetyllactosamine, which is synthesized by I-bran
59 poorly to beta1,6-GlcNAc attached to linear poly-N-acetyllactosamines, while beta1, 3-N-acetylglucos
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