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1 Heparanase is a heparan sulfate degrading endoglycosidase.
2 ns are first deglycosylated with a wild-type 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
7 ompounds were identified by a combination of endoglycosidase and exoglycosidase digestions, anion-exc
8 ng advantage of the specificity of different endoglycosidases and isotope dimethyl labeling, six N-gl
9 ere determined by treating each protein with endoglycosidases and then subjecting it to sodium dodecy
12 o mutants described here represent the first endoglycosidase-based glycosynthases enabling a highly e
13 In this article, we report studies of two endoglycosidase-based glycosynthases, EndoM-N175A and En
14 from Streptococcus pneumoniae (Endo-D) is an endoglycosidase capable of hydrolyzing the Fc N-glycan o
15 fringens ATCC10543 were contaminated with an endoglycosidase capable of releasing the disaccharide Gl
17 We describe herein the optimization of an endoglycosidase-catalyzed glycosylation of the best-sell
18 ha-mannosidase inhibitor kifunensine, and an endoglycosidase-catalyzed glycosylation of the deglycosy
20 in vitro enzymatic glycosylation, using the endoglycosidase-catalyzed transglycosylation as the key
21 e containing two GlcNAc residues and a novel endoglycosidase-catalyzed transglycosylation that simult
22 the GlcNAc-primer in the IgG1-Fc through an endoglycosidase-catalyzed transglycosylation, using suga
25 eral hours to overnight) and relatively high endoglycosidase concentration (from 1:250 to 1:500 enzym
26 d here provides a framework from which novel endoglycosidases could be engineered for additional clin
27 utant TREM2 becomes sensitive to cleavage by endoglycosidase D under conditions that inhibit recyclin
30 sylation, in contrast to previously reported endoglycosidases derived from Endo-S, Endo-M, Endo-D, an
33 ither tunicamycin treatment of the cells nor endoglycosidase digestion of calreticulin resulted in an
34 lation process inhibitor kifunensine and the endoglycosidase Endo H, and intramuscularly immunized mi
35 We identified an 88-kDa secreted protein, endoglycosidase (Endo) E, which is most likely responsib
36 nes , EndoS, is complementary to other known endoglycosidases (EndoA, EndoH) used for current protein
37 ities of the bacterial protease IdeS and the endoglycosidase EndoS, upregulated during infection.
39 analysis using a combination of IdeS and the endoglycosidases EndoS and EndoS2 to comprehensively map
40 ost common human pathogens, secretes a large endoglycosidase, EndoS, which removes carbohydrates in a
42 icken erythroid AE1 anion exchangers receive endoglycosidase F (endo F)-sensitive sugar modifications
43 CD38 HL-60 ADPR-cyclase to inactivation by N-endoglycosidase F and to thermal inactivation at 45 degr
44 ectants after removal of sugar residues with endoglycosidase F or following tunicamycin treatment to
45 und to be resistant to digestion with either endoglycosidase F or H but sensitive to peptide N-glycos
46 with high concentrations of N-glycosidase F, endoglycosidase F, endoglycosidase H, and endo-beta-gala
51 protein) which was sensitive to tunicamycin, endoglycosidase F/N-glycosidase, and endoglycosidase H b
52 cted by treatment of the cells with trypsin, endoglycosidase F/peptide N-glycosidase F, Vibrio choler
57 sidase assisted analysis using sialidase and endoglycosidase F2/F3, respectively, to improve resoluti
58 labeled with 2-aminobenzamide, digested with Endoglycosidases F2 and H followed by normal phase HPLC
60 derived from Elizabethkingia meningoseptica endoglycosidase F3 (Endo-F3) of the GH18 family, which a
61 n was determined for core fucosylation using endoglycosidase F3, and differentiation of sialic acid l
62 ed by site-directed mutagenesis of EndoS (an endoglycosidase from Streptococcus pyogenes ) and were f
64 a systematic site-directed mutagenesis of an endoglycosidase from Streptococcus pyogenes of serotype
69 lex (pgCIII) was sensitive to treatment with endoglycosidase H (endo H), while the mature gCIII compl
71 pike protein (S) was newly synthesized as an endoglycosidase H (endo H)-sensitive glycoprotein (gp170
72 n-19 is not utilized; Asn-39 is linked to an endoglycosidase H (Endo H)-sensitive oligosaccharide, an
79 onnatural sugars at N-glycan core positions, endoglycosidase H (endoH)-digested peptides from a purif
80 nt molecular weights and remained completely endoglycosidase H (endoH)-sensitive, suggesting incomple
81 val, (ii) all detectable processed mMDC15 is endoglycosidase H -resistant, and (iii) a recombinant so
86 cognized by this antiserum were sensitive to endoglycosidase H and associated with calnexin, indicati
87 igomers; however, they remained sensitive to endoglycosidase H and did not undergo endoproteolytic cl
91 nous parasite glycoproteins using sequential endoglycosidase H and peptide:N-glycosidase-F digestions
93 US7, US9, and US10 remained sensitive to endoglycosidase H and were exclusively or largely presen
94 CPD increases to 180 kDa and is resistant to endoglycosidase H as a result of carbohydrate maturation
95 PP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with
97 , and both mature proteins were resistant to endoglycosidase H but sensitive to glycopeptidase F.
101 y limited trypsin digestion and treated with endoglycosidase H deglycosidase to reduce heterogeneity
104 but in alpha1(A322D)beta2gamma2S receptors, endoglycosidase H deglycosylated 91 +/- 4% of alpha1(A32
106 However, cell surface biotinylation and endoglycosidase H digestion assays appear to under-repre
108 n sensitivity to both mannan competition and endoglycosidase H digestion compared to that of the 124m
112 on of flow cytometry, patch clamp recording, endoglycosidase H digestion, brefeldin A treatment, and
114 elet Mpl, PV platelet Mpl was susceptible to endoglycosidase H digestion, indicating defective Mpl pr
115 gglutinin at a stage preceding resistance to endoglycosidase H digestion, thus impairing hemagglutini
121 tution mutant S proteins displayed levels of endoglycosidase H resistance and cell surface expression
122 se media reversibly inhibited development of endoglycosidase H resistance and mannose-binding activit
123 ldin A required more than 120 min to acquire endoglycosidase H resistance and maximal binding activit
124 slational processing of these two mutants to endoglycosidase H resistance and very low cell surface e
125 e cell surface have the potential to acquire endoglycosidase H resistance as a consequence of Golgi-b
126 he ER is confirmed by the failure to acquire endoglycosidase H resistance at 37 degrees C and cannot
127 al approach, we found that the onset of VSVG endoglycosidase H resistance in Rab6 depleted cells was
129 D deglycosylated with endoglycosidase F2 and endoglycosidase H retained ANP-binding activity and show
130 leavage site mutant I was N glycosylated and endoglycosidase H sensitive, indicating that ER transloc
131 cular chaperones BiP and GRP94, and remained endoglycosidase H sensitive, suggesting retention in the
132 emonstrated that the M(r) 85,000 species was endoglycosidase H sensitive, suggesting targeting of the
134 munofluorescence microscopy and constitutive endoglycosidase H sensitivity in metabolically labeled c
135 between the two cell lines as determined by endoglycosidase H sensitivity of newly sensitized P-glyc
139 tor N-butyldeoxynojirimycin and treated with endoglycosidase H to remove all but the terminal N-acety
141 d material to dense lysosomes was delayed in endoglycosidase H treated cells, but the rate of degrada
142 Pulse-chase experiments in combination with endoglycosidase H treatment determined that the mutant m
144 d be inhibited by d-mannose and abolished by endoglycosidase H treatment of THP, suggesting that the
147 In addition to transcription/translation, endoglycosidase H treatment was used to verify glycosyla
149 ion, we determined that N-glycan removal via endoglycosidase H(f) treatment of TconTS1 led to a decre
150 and only the 93-kDa wt C2 were sensitive to endoglycosidase H, a marker for transport from the endop
152 ith neuraminidase, resistance to cleavage by endoglycosidase H, and GalNAc-independent labeling with
153 mutant receptor to peptide-N-glycanase F and endoglycosidase H, and insensitivity to sialidase indica
155 porate the J chain and resist degradation by endoglycosidase H, arguing for IgM passage through the G
156 from mPmel17 not only in its sensitivity to endoglycosidase H, but also in the content of core 1 O-g
159 ome processed fertilin alpha is sensitive to endoglycosidase H, suggesting cleavage occurs prior to t
160 lted in some enzyme that lost sensitivity to endoglycosidase H, suggesting that the first disulfide b
161 TR-infected cells, gO remained sensitive to endoglycosidase H, suggesting that the protein was not e
162 toreceptors, P/rds was robustly sensitive to endoglycosidase H, which is consistent with its bypassin
164 The structures, determined at 1.85 A for the endoglycosidase H-deglycosylated protease domain produce
165 n the Cbeta domain, was thrombin-cleaved and endoglycosidase H-digested, and the two derivatives were
166 ecules are delayed in their maturation to an endoglycosidase H-resistant form after biosynthetic labe
167 ed ADAM3 exhibited an increased amount of an endoglycosidase H-resistant form that may be related to
168 nverted to the Golgi-processed and therefore endoglycosidase H-resistant form, and the endoglycosidas
169 he Ostalpha subunit to a mature glycosylated endoglycosidase H-resistant form, suggesting that co-exp
174 pancies of numerous N-glycosylation sites by endoglycosidase H-resistant N-glycans originating from M
177 cosylation sites and unknown numbers of both endoglycosidase H-sensitive and -resistant oligosacchari
179 l cytoplasmic domain show that they exit the endoglycosidase H-sensitive compartment at a slower rate
180 x glycosylation of wild-type AQP2 but mainly endoglycosidase H-sensitive core glycosylation of AQP2-T
181 re endoglycosidase H-resistant form, and the endoglycosidase H-sensitive ER form has a half-life of 2
182 retained in the endoplasmic reticulum in an endoglycosidase H-sensitive form associated with the mol
183 rbohydrate chains of SCAP were mostly in the endoglycosidase H-sensitive form when cells were grown i
184 s of S and MHVR via coimmunoprecipitation of endoglycosidase H-sensitive forms of the two proteins.
188 sed surface IgM coupled with accumulation of endoglycosidase H-sensitive IgM intracellularly, resembl
189 NAc2-PP-dolichol transferred by TbSTT3A, and endoglycosidase H-sensitive N-glycans originating from M
190 ocol; describes the presence of full-length, endoglycosidase H-sensitive NSP4 in plasma membrane cave
192 d-type gE were synthesized as N-glycosylated endoglycosidase H-sensitive precursors with approximate
194 peared mostly as a 70-kDa core-glycosylated, endoglycosidase H-sensitive, immature form bound to the
200 s a 45-kDa glycoprotein that is sensitive to endoglycosidase-H and is reduced to 37-kDa after N-glyca
202 ling studies demonstrate that acquisition of endoglycosidase-H resistance of CD1d is observed in the
203 cells, however, Glyco-PDIA1 is released with endoglycosidase-H sensitive glycans, implying that it do
204 and gamma(c) chains associated with p12I are endoglycosidase-H sensitive, suggesting that their inter
206 es, but the currently limited selectivity of endoglycosidases has prevented effective manipulation of
208 ell-associated molecules leads to sequential endoglycosidase (heparanase) fragmentation of the chains
209 dels to investigate the contributions of the endoglycosidase HYAL1 and the exoglycosidase beta-hexosa
210 Introduction of both the engineered mAb and endoglycosidase in serum leads to a dramatic increase in
212 ectivity for amylases over related retaining endoglycosidases is validated by structural studies.
213 cellular production of functional vIL-6, but endoglycosidase-mediated removal of N-linked glycans fro
214 eless, neither Endo-A nor the Mucor hiemalis endoglycosidase mutants (EndoM-N175A and EndoM-N175Q) we
215 pact on antibody effector function, with the endoglycosidases of Streptococcus pyogenes deglycosylati
226 dentified by molecular weight determination, endoglycosidase sensitivity, and microsequencing analysi
231 Heparanase (HPSE) is the sole mammalian endoglycosidase that degrades heparan sulfate (HS) prote
232 Gs can be cleaved by HPR1 (heparanase-1), an endoglycosidase that is overexpressed in many types of m
233 Hyaluronidase is a hyaluronic acid-degrading endoglycosidase that is present in many toxins and the l
237 based proteomics strategy that uses specific endoglycosidases to introduce mass signatures that disti
241 mutagenesis of the glycosylation site or by endoglycosidase treatment, reduced receptor activation.