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1 iles of N-glycans enzymatically treated with fucosidase.
2 es carrying a BODIPY fluorophore for alpha-l-fucosidase.
3 ctosidase, alpha-L-arabinosidase and alpha-L-fucosidase.
4 c) or by pretreatment of cells with alpha1-2 fucosidase.
5 d molecules, fucose metabolism and two alpha-fucosidases.
6 cattering in contrast to reported multimeric fucosidases.
7 To improve upon previous assays for alpha-l-fucosidase, a fluorescence based immunoassay was produce
9 rans-beta-galactosidase (but not trans-alpha-fucosidase) activities that graft sugar residues from on
10 ctosidase (BGAL) variants with enhanced beta-fucosidase activity (tenfold increase in k(cat)/K(M) in
13 ase that also shows beta-galactosidase, beta-fucosidase, alpha-arabinofuranosidase, and alpha-arabino
16 lity of [(14)C]fucosylated AGPs to alpha(1,2)fucosidase, and not to alpha(1,3/4)fucosidase, indicated
17 e calibration curves for quantifying alpha-l-fucosidase concentrations in both PBS and human blood se
18 sylation of glycoproteins using alpha(1-3,4)-fucosidase, endo-beta-galactosidase, and PNGase F disrup
19 glycoside hydrolase family 29 (GH29) alpha-L-fucosidase from plant pathogenic fungus Fusarium gramine
26 due E274 of the Lactobacillus casei alpha1,6-fucosidase, including E274A, E274S, and E274G, acted as
27 alpha(1,2)fucosidase, and not to alpha(1,3/4)fucosidase, indicated that an alpha(1,2) linkage is form
30 trate specificity revealed that the alpha1,6-fucosidase mutants could introduce an alpha1,6-fucose mo
31 r CHO and COS), pBK-RSV-tyrosinase, and pCP4-fucosidase plasmids, respectively, by electroporation in
35 when systemic cells were treated with alpha-fucosidase, suggesting that the GlcNAc beta 1-4GlcNAc mo
36 screening enabled the identification of beta-fucosidases that are significantly more active (180-fold
37 cteroides thetaiotaomicron produces multiple fucosidases that cleave fucose from host glycans, result
38 0 amino acids were constructed as artificial fucosidases that exhibit selective carbohydrate cleavage
41 L-fucose, which we confirmed by showing that fucosidase-treated cells, largely, failed to activate co
43 D-galactosidase, beta-D-galactosidase, alpha-fucosidase, trypsin-like activity, and chymotrypsin was
44 of a glycoside hydrolase family GH29 alpha-L-fucosidase unveiling a Michaelis (ES) complex in a (1)C(
47 most closely resembles inverting GH95 alpha-fucosidase, which displays the highest specificity with
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