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1                           While the N-beta-d-glucosaminyl 1,2,3-triazoles showed weak or no inhibitio
2 saminyl)-1,2,3-triazoles as well as C-beta-d-glucosaminyl 1,2,4-triazoles and imidazoles were synthes
3                   Aryl substituted 1-(beta-d-glucosaminyl)-1,2,3-triazoles as well as C-beta-d-glucos
4 ibility, we synthesized 4-O-(N-acetyl-beta-d-glucosaminyl)-1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-
5 omposed of the long sought heparan sulfate D-glucosaminyl 3-O-sulfotransferase (3-OST).
6 ulfation of glucosamine by heparan sulfate D-glucosaminyl 3-O-sulfotransferase (3-OST-1) is the key m
7  and molecularly clone the heparan sulfate D-glucosaminyl 3-O-sulfotransferase (3-OST-1), which is th
8          Here we show that heparan sulfate D-glucosaminyl 3-O-sulfotransferase 2 (HS3ST-2) is a marke
9        Two of these genes, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1 and hyaluronan syn
10 matrix metallopeptidase 2, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1, and hyaluronan sy
11 omponent was identified as heparan sulfate D-glucosaminyl 3-O-sulfotransferase because it transferred
12 t activity to heparin, and HS3ST3A1, another glucosaminyl 3-O-sulfotransferase expressed in cells.
13 lfate modified by a subset of the multiple D-glucosaminyl 3-O-sulfotransferase isoforms provides site
14  the rate-limiting enzyme, heparan sulfate D-glucosaminyl 3-O-sulfotransferase-1 (3-OST-1) (EC 2.8.2.
15 coagulant heparan sulfate, the cDNA encoding glucosaminyl 3-O-sulfotransferase-1 (3-OST-1) was introd
16 e residue in an immobilized HS chain using D-glucosaminyl 3-O-sulfotransferase.
17 3-OST-3A, and 3-OST-3B are heparan sulfate D-glucosaminyl 3-O-sulfotransferases because the enzymes t
18 ulfate is generated by the heparan sulfate d-glucosaminyl-3-O-sulfotransferase isoform 3 (3-OST-3), a
19 ty, and the best inhibitor was the 2-(beta-d-glucosaminyl)-4(5)-(2-naphthyl)-imidazole with a Ki valu
20  due to coupling of uronyl 2-O-sulfation and glucosaminyl 6-O-sulfation to initial N-deacetylation an
21 uronyl 2-O-sulfotransferase (Hs2st(f/f)) and glucosaminyl 6-O-sulfotransferase-1 (Hs6st1(f/f)) and th
22  glucosamine residues, which is generated by glucosaminyl-6-O-sulfotransferases (HS6STs) and selectiv
23 ells accumulate Man5GlcNAc2-P-P-dolichol and glucosaminyl-acylphosphatidylinositol.
24                               In this group, glucosaminyl(alpha 1-->6)-D-myo-inositol inhibited more
25 nose and hybrid, peptide-N(4)-(N-acetyl-beta-glucosaminyl) Asn amidase (EC 3.5.1.52)-released complex
26 y to analyze the peptide-N4-(N-acetyl-beta-D-glucosaminyl)asparagine amidase (PNGase F)- and endo-bet
27 ew glycoamidase, peptide-N4-(N-acetyl-beta-D-glucosaminyl)asparagine amidase (PNGase) At, was discove
28     Glycoamidases (peptide-N4-(N-acetyl-beta-glucosaminyl)asparagine amidase, EC 3.5.1.52; also known
29  carbohydrate consisting of beta1,3 N-acetyl glucosaminyl-beta1,4 glucuronide.
30 s in inhibitory potency between glucosyl and glucosaminyl derivatives and also for the differences be
31 s showed weak or no inhibition, the C-beta-d-glucosaminyl derivatives had potent activity, and the be
32 d set of orthogonal protecting groups on a D-glucosaminyl donor.
33 ker disaccharide [rhamnosyl (Rha) - N-acetyl-glucosaminyl (GlcNAc) phosphate] on the decaprenyl-phosp
34 NAcLc(3)Cer and recognizes the terminal beta-glucosaminyl (GlcNH(2)) residue, having a free NH(2) gro
35  a glycoprotein with exposed N-acetyl-beta-D-glucosaminyl groups, (iii) P. marneffei stimulates the r
36  anthracis, which combine to produce alpha-d-glucosaminyl l-malate (GlcN-malate) from UDP-GlcNAc and
37                                          The glucosaminyl N-deacetylase/N-sulfotransferase (NDST) enz
38 ructures is likely governed by the action of glucosaminyl N-deacetylase/N-sulfotransferase (NDST).
39 d within a regulatory region upstream of the glucosaminyl (N-acetyl) transferase 2 (GCNT2) gene and c
40                     Mutation analysis of the glucosaminyl (N-acetyl) transferase 2 gene (GCNT2) gene
41          Expression of carbonic anhydrase I, glucosaminyl (N-acetyl) transferase 2, and miR-96 (three
42 , we have showed that GCNT2, a gene-encoding glucosaminyl (N-acetyl) transferase 2, I-branching enzym
43  A3 (Foxa3), anterior gradient 2 (Agr2), and glucosaminyl (N-acetyl) transferase 3, mucin type (Gcnt3
44 nosylation of the glucosamine residue of the glucosaminyl phosphatidylinositol (GlcNalpha-PI) interme
45 1,6-L-fucosyl residue located on the distant glucosaminyl residue that is directly attached to the as
46       The formation of IdUA and 6-O-sulfated glucosaminyl residues appears to be independent of 2-O-s
47                                 3-O-Sulfated glucosaminyl residues are rare constituents of heparan s
48 ing beta-D-glucuronosyl and N-acetyl-alpha-D-glucosaminyl residues by exostosins.
49 zymes confirms the 3-O-sulfation of specific glucosaminyl residues within heparan sulfate.