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1 ns are first deglycosylated with a wild-type endoglycosidase.
2 Heparanase is a heparan sulfate degrading endoglycosidase.
3 in SDS-PAGE before and after treatment with endoglycosidase.
5 lglucosamine (GlcNAc) of IgG, using a mutant endoglycosidase (also called endoglycosynthase) that lac
6 ompounds were identified by a combination of endoglycosidase and exoglycosidase digestions, anion-exc
7 ere determined by treating each protein with endoglycosidases and then subjecting it to sodium dodecy
10 o mutants described here represent the first endoglycosidase-based glycosynthases enabling a highly e
11 In this article, we report studies of two endoglycosidase-based glycosynthases, EndoM-N175A and En
12 from Streptococcus pneumoniae (Endo-D) is an endoglycosidase capable of hydrolyzing the Fc N-glycan o
13 fringens ATCC10543 were contaminated with an endoglycosidase capable of releasing the disaccharide Gl
15 We describe herein the optimization of an endoglycosidase-catalyzed glycosylation of the best-sell
16 ha-mannosidase inhibitor kifunensine, and an endoglycosidase-catalyzed glycosylation of the deglycosy
18 in vitro enzymatic glycosylation, using the endoglycosidase-catalyzed transglycosylation as the key
19 e containing two GlcNAc residues and a novel endoglycosidase-catalyzed transglycosylation that simult
20 the GlcNAc-primer in the IgG1-Fc through an endoglycosidase-catalyzed transglycosylation, using suga
23 eral hours to overnight) and relatively high endoglycosidase concentration (from 1:250 to 1:500 enzym
24 d here provides a framework from which novel endoglycosidases could be engineered for additional clin
25 utant TREM2 becomes sensitive to cleavage by endoglycosidase D under conditions that inhibit recyclin
28 sylation, in contrast to previously reported endoglycosidases derived from Endo-S, Endo-M, Endo-D, an
31 ither tunicamycin treatment of the cells nor endoglycosidase digestion of calreticulin resulted in an
32 We identified an 88-kDa secreted protein, endoglycosidase (Endo) E, which is most likely responsib
33 nes , EndoS, is complementary to other known endoglycosidases (EndoA, EndoH) used for current protein
34 analysis using a combination of IdeS and the endoglycosidases EndoS and EndoS2 to comprehensively map
35 ost common human pathogens, secretes a large endoglycosidase, EndoS, which removes carbohydrates in a
36 icken erythroid AE1 anion exchangers receive endoglycosidase F (endo F)-sensitive sugar modifications
37 CD38 HL-60 ADPR-cyclase to inactivation by N-endoglycosidase F and to thermal inactivation at 45 degr
38 ectants after removal of sugar residues with endoglycosidase F or following tunicamycin treatment to
39 und to be resistant to digestion with either endoglycosidase F or H but sensitive to peptide N-glycos
40 with high concentrations of N-glycosidase F, endoglycosidase F, endoglycosidase H, and endo-beta-gala
45 protein) which was sensitive to tunicamycin, endoglycosidase F/N-glycosidase, and endoglycosidase H b
46 cted by treatment of the cells with trypsin, endoglycosidase F/peptide N-glycosidase F, Vibrio choler
51 sidase assisted analysis using sialidase and endoglycosidase F2/F3, respectively, to improve resoluti
52 labeled with 2-aminobenzamide, digested with Endoglycosidases F2 and H followed by normal phase HPLC
54 derived from Elizabethkingia meningoseptica endoglycosidase F3 (Endo-F3) of the GH18 family, which a
55 ed by site-directed mutagenesis of EndoS (an endoglycosidase from Streptococcus pyogenes ) and were f
57 a systematic site-directed mutagenesis of an endoglycosidase from Streptococcus pyogenes of serotype
61 lex (pgCIII) was sensitive to treatment with endoglycosidase H (endo H), while the mature gCIII compl
63 pike protein (S) was newly synthesized as an endoglycosidase H (endo H)-sensitive glycoprotein (gp170
64 n-19 is not utilized; Asn-39 is linked to an endoglycosidase H (Endo H)-sensitive oligosaccharide, an
71 onnatural sugars at N-glycan core positions, endoglycosidase H (endoH)-digested peptides from a purif
72 nt molecular weights and remained completely endoglycosidase H (endoH)-sensitive, suggesting incomple
73 val, (ii) all detectable processed mMDC15 is endoglycosidase H -resistant, and (iii) a recombinant so
78 cognized by this antiserum were sensitive to endoglycosidase H and associated with calnexin, indicati
79 igomers; however, they remained sensitive to endoglycosidase H and did not undergo endoproteolytic cl
83 nous parasite glycoproteins using sequential endoglycosidase H and peptide:N-glycosidase-F digestions
85 US7, US9, and US10 remained sensitive to endoglycosidase H and were exclusively or largely presen
86 CPD increases to 180 kDa and is resistant to endoglycosidase H as a result of carbohydrate maturation
87 PP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with
89 , and both mature proteins were resistant to endoglycosidase H but sensitive to glycopeptidase F.
93 y limited trypsin digestion and treated with endoglycosidase H deglycosidase to reduce heterogeneity
96 but in alpha1(A322D)beta2gamma2S receptors, endoglycosidase H deglycosylated 91 +/- 4% of alpha1(A32
100 n sensitivity to both mannan competition and endoglycosidase H digestion compared to that of the 124m
104 on of flow cytometry, patch clamp recording, endoglycosidase H digestion, brefeldin A treatment, and
106 elet Mpl, PV platelet Mpl was susceptible to endoglycosidase H digestion, indicating defective Mpl pr
107 gglutinin at a stage preceding resistance to endoglycosidase H digestion, thus impairing hemagglutini
112 tution mutant S proteins displayed levels of endoglycosidase H resistance and cell surface expression
113 se media reversibly inhibited development of endoglycosidase H resistance and mannose-binding activit
114 ldin A required more than 120 min to acquire endoglycosidase H resistance and maximal binding activit
115 slational processing of these two mutants to endoglycosidase H resistance and very low cell surface e
116 e cell surface have the potential to acquire endoglycosidase H resistance as a consequence of Golgi-b
117 he ER is confirmed by the failure to acquire endoglycosidase H resistance at 37 degrees C and cannot
119 D deglycosylated with endoglycosidase F2 and endoglycosidase H retained ANP-binding activity and show
120 leavage site mutant I was N glycosylated and endoglycosidase H sensitive, indicating that ER transloc
121 cular chaperones BiP and GRP94, and remained endoglycosidase H sensitive, suggesting retention in the
122 emonstrated that the M(r) 85,000 species was endoglycosidase H sensitive, suggesting targeting of the
124 munofluorescence microscopy and constitutive endoglycosidase H sensitivity in metabolically labeled c
125 between the two cell lines as determined by endoglycosidase H sensitivity of newly sensitized P-glyc
129 tor N-butyldeoxynojirimycin and treated with endoglycosidase H to remove all but the terminal N-acety
131 d material to dense lysosomes was delayed in endoglycosidase H treated cells, but the rate of degrada
132 Pulse-chase experiments in combination with endoglycosidase H treatment determined that the mutant m
134 d be inhibited by d-mannose and abolished by endoglycosidase H treatment of THP, suggesting that the
137 In addition to transcription/translation, endoglycosidase H treatment was used to verify glycosyla
139 and only the 93-kDa wt C2 were sensitive to endoglycosidase H, a marker for transport from the endop
141 ith neuraminidase, resistance to cleavage by endoglycosidase H, and GalNAc-independent labeling with
142 mutant receptor to peptide-N-glycanase F and endoglycosidase H, and insensitivity to sialidase indica
144 porate the J chain and resist degradation by endoglycosidase H, arguing for IgM passage through the G
145 from mPmel17 not only in its sensitivity to endoglycosidase H, but also in the content of core 1 O-g
148 ome processed fertilin alpha is sensitive to endoglycosidase H, suggesting cleavage occurs prior to t
149 lted in some enzyme that lost sensitivity to endoglycosidase H, suggesting that the first disulfide b
150 TR-infected cells, gO remained sensitive to endoglycosidase H, suggesting that the protein was not e
151 toreceptors, P/rds was robustly sensitive to endoglycosidase H, which is consistent with its bypassin
153 The structures, determined at 1.85 A for the endoglycosidase H-deglycosylated protease domain produce
154 n the Cbeta domain, was thrombin-cleaved and endoglycosidase H-digested, and the two derivatives were
155 ecules are delayed in their maturation to an endoglycosidase H-resistant form after biosynthetic labe
156 ed ADAM3 exhibited an increased amount of an endoglycosidase H-resistant form that may be related to
157 nverted to the Golgi-processed and therefore endoglycosidase H-resistant form, and the endoglycosidas
158 he Ostalpha subunit to a mature glycosylated endoglycosidase H-resistant form, suggesting that co-exp
163 pancies of numerous N-glycosylation sites by endoglycosidase H-resistant N-glycans originating from M
166 cosylation sites and unknown numbers of both endoglycosidase H-sensitive and -resistant oligosacchari
168 l cytoplasmic domain show that they exit the endoglycosidase H-sensitive compartment at a slower rate
169 x glycosylation of wild-type AQP2 but mainly endoglycosidase H-sensitive core glycosylation of AQP2-T
170 re endoglycosidase H-resistant form, and the endoglycosidase H-sensitive ER form has a half-life of 2
171 retained in the endoplasmic reticulum in an endoglycosidase H-sensitive form associated with the mol
172 rbohydrate chains of SCAP were mostly in the endoglycosidase H-sensitive form when cells were grown i
173 s of S and MHVR via coimmunoprecipitation of endoglycosidase H-sensitive forms of the two proteins.
177 sed surface IgM coupled with accumulation of endoglycosidase H-sensitive IgM intracellularly, resembl
178 NAc2-PP-dolichol transferred by TbSTT3A, and endoglycosidase H-sensitive N-glycans originating from M
179 ocol; describes the presence of full-length, endoglycosidase H-sensitive NSP4 in plasma membrane cave
181 d-type gE were synthesized as N-glycosylated endoglycosidase H-sensitive precursors with approximate
183 peared mostly as a 70-kDa core-glycosylated, endoglycosidase H-sensitive, immature form bound to the
189 s a 45-kDa glycoprotein that is sensitive to endoglycosidase-H and is reduced to 37-kDa after N-glyca
191 ling studies demonstrate that acquisition of endoglycosidase-H resistance of CD1d is observed in the
192 and gamma(c) chains associated with p12I are endoglycosidase-H sensitive, suggesting that their inter
194 es, but the currently limited selectivity of endoglycosidases has prevented effective manipulation of
196 ell-associated molecules leads to sequential endoglycosidase (heparanase) fragmentation of the chains
197 dels to investigate the contributions of the endoglycosidase HYAL1 and the exoglycosidase beta-hexosa
198 Introduction of both the engineered mAb and endoglycosidase in serum leads to a dramatic increase in
200 cellular production of functional vIL-6, but endoglycosidase-mediated removal of N-linked glycans fro
201 eless, neither Endo-A nor the Mucor hiemalis endoglycosidase mutants (EndoM-N175A and EndoM-N175Q) we
209 dentified by molecular weight determination, endoglycosidase sensitivity, and microsequencing analysi
214 Gs can be cleaved by HPR1 (heparanase-1), an endoglycosidase that is overexpressed in many types of m
215 Hyaluronidase is a hyaluronic acid-degrading endoglycosidase that is present in many toxins and the l
218 based proteomics strategy that uses specific endoglycosidases to introduce mass signatures that disti
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