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1 ulfation of glucosamine residues rather than iduronate 2-O-sulfation being important for bioactivity.
2 A signal peptide sequence with that of human iduronate 2-sulfatase (IDS) achieved higher transgene ex
3 two distinct TfR-targeted platforms fused to iduronate 2-sulfatase (IDS), a lysosomal enzyme deficien
6 ed a tandem mass spectrometry based assay of iduronate-2-sulfatase (IdS) activity for the neonatal de
7 om alpha-L-iduronidase (IDUA) deficiency and iduronate-2-sulfatase (IDS) deficiency, respectively.
9 I subject had a transient increase in plasma iduronate-2-sulfatase approaching normal levels and one
10 caused by mutations in the IDS gene encoding iduronate-2-sulfatase, a crucial enzyme in the lysosomal
11 strates for the enzymes alpha-l-iduronidase, iduronate-2-sulfatase, and N-acetylgalactosamine-4-sulfa
12 the higher-order structures in idursulfase (iduronate-2-sulfatase, I2S) has been accomplished throug
14 etic substrate (IdS-S) consisting of alpha-L-iduronate-2-sulfate, which is glycosidically conjugated
19 teresting interplay between requirements for iduronate and sulfate density that may reflect in part a
20 ulfation of hexosamines and 2-O-sulfation of iduronates are not absolute requirements for glycosamino
22 ts as a conformational switch to superdisarm iduronate components, reversible by lactone ring opening
23 e binding site in the protein to accommodate iduronate-containing sequences of variable sulfation pat
25 te enables short, scalable syntheses of an L-iduronate diacetate C-4 acceptor, and also L-iduronate C
26 adopt (1)C(4) conformations in solution, the iduronate ester adopts the (4)C(1) conformation in solid
27 fated trisaccharide comprised of an internal iduronate flanked by monosulfated hexosamine residues an
29 conformationally locked bicyclic 1,6-anhydro iduronate lactone along with an X-ray structures of a no
30 X-ray structures are reported for a [2.2.2] iduronate lactone and examples of both methyl L-idopyran
32 nase I-like, cleaving at hexosamine-sulfated iduronate linkages, whereas the other is presumably hepa
34 digests of heparin that contains a Delta-2S-iduronate on the non-reducing end does not initiate the
35 rbation of the conformational equilibrium of iduronate residue G through replacement of the nonessent
43 lfate fine structure, where highly sulfated, iduronate-rich domains alternate with N-acetylated domai
44 rs endows these chains with highly sulfated, iduronate-rich regions, which are major determinants of
46 from 1 to a new type of highly disarmed O-4 iduronate thioglycoside, which is an effective acceptor
47 arin, and (iii) that removal of the Delta-2S-iduronate to expose the fully sulfated trisaccharide (Gl
48 e of glucosamine, but not the 2-O-sulfate of iduronate within heparin is required for 3Q binding, ind