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1 to treatment of macrophages with trypsin or heparinase.
2 PG and in HSPG-expressing cells treated with heparinase.
3 sensitive to both chondroitin ABC lyase and heparinase.
4 main, and by incubating the blastocysts with heparinase.
5 excess heparan sulfate and by treatment with heparinase.
6 sion was reversed by tetrahydrolipstatin and heparinase.
7 which was reversed by antifibrinolytics and heparinase.
8 y soluble heparin and by treating cells with heparinase.
9 rin or by the pretreatment of the cells with heparinase.
10 bolished when CHO-K1 cells were treated with heparinases.
11 ycosaminoglycans (GAGs) on the action of the heparinases.
12 broadest known substrate specificity of the heparinases.
13 age of entry was observed in CF treated with heparinases.
14 , however, contained three, compared to two, heparinase 1-resistant sequences separated by larger con
17 ell surface heparan sulfate proteoglycans by heparinase and heparitinase but not by treatment with co
18 with the glycosaminoglycan-degrading enzymes heparinase and heparitinase suggesting the specific invo
19 was examined with or without the addition of heparinase and heparitinase to cell incubation mixtures.
21 rin formation) greater than 1 minute between heparinase and standard thrombelastogram (TEG) is associ
23 on of heparin-like glycosaminoglycans by the heparinases and mutant heparinases could pave the way to
24 By disrupting (with sulfation inhibitors and heparinase) and partially reconstituting (with heparin)
25 ls and primary neurons by heparin, chlorate, heparinase, and genetic knockdown of a key HSPG syntheti
27 -like glycosaminoglycan degrading enzymes or heparinases are powerful tools that have enabled the elu
28 of porcine intestinal heparin with bacterial heparinase), as well as a heparin-derived pharmaceutical
31 anced uptake was reduced by more than 80% by heparinase but was unaffected by the 39-kDa protein.
34 cess heparin or pretreatment of acini with a heparinase cocktail each inhibited Ad5 transduction by a
35 minating heparan sulfate proteoglycans using heparinase completely abrogated the mechanical induction
36 g distinctions in substrate specificities of heparinases could be used to isolate oligosaccharides wi
37 osaminoglycans by the heparinases and mutant heparinases could pave the way to the development of muc
38 independent means of disrupting syndecan-4: heparinase degradation of HS glycosaminoglycans or suppr
42 increased binding of both proteins, whereas heparinase digestion and competition with heparin/HS inh
43 pressing activity of EHS-BM was sensitive to heparinase digestion but not to chondroitinase ABC or hy
44 assay to assess the purity of heparin using heparinase digestion followed by size-exclusion HPLC ana
48 tease (EC 3.4.21.16); (iv) lyase activity of heparinase (EC 4.1.1.7); and (v) ligase activity of pyru
51 zation, while pretreatment of HIS cells with heparinase enzyme or with anti-3-OS HS (G2) peptide sign
54 Heparinase III is the unique member of the heparinase family of heparin-degrading lyases that recog
57 ools used for the production of LMWH are the heparinases from Flavobacterium heparinum, specifically
59 polymerization using the bacterially derived heparinases, given the structural understanding of their
61 noglycans and treatment of target cells with heparinase had no significant inhibition on cytoadherenc
68 t, but did not change the product profile of heparinase I action on heparin; conversely, mutations in
71 raphy suggested that mutations in CB-1 alter heparinase I activity primarily through decreasing the e
72 nt, but they had a more pronounced effect on heparinase I activity, suggesting a different role for C
76 ride, we showed that the interaction between heparinase I and calcium was essential for proper functi
77 ave shown that calcium binds specifically to heparinase I and have identified two major calcium-bindi
80 xperiments to answer the question of whether heparinase I binds to calcium and, if so, which regions
81 , strongly suggests that the inactivation of heparinase I by DEPC is specific for histidine residues.
83 to further understand the mechanism by which heparinase I cleaves its polymer substrate, we sought to
84 also identified a heparin binding domain in heparinase I containing two positively charged clusters
86 stions with individual enzymes revealed that heparinase I did not cleave at GlcNH(3)(+) residues; how
94 erve concentration-dependent inactivation of heparinase I in the presence of reversible histidine-mod
95 bonate (DEPC); 0.3 mM DEPC results in 95% of heparinase I inactivation in less than 3 min, and as low
98 hydryl selective labeling of cysteine 135 of heparinase I protects the lysines of the heparin binding
99 Pretreatment of monocytes with heparin or heparinase I resulted in partial inhibition of cell adhe
100 us to propose a model for calcium binding to heparinase I that includes both CB-1 and CB-2 providing
101 nd competition assays, to map the regions of heparinase I that interact specifically with heparin.
102 (Glu207-Ala219) and CB-2 (Thr373-Arg384), in heparinase I that not only are specifically modified by
103 heparin binding site, may bridge heparin to heparinase I through calcium in a ternary complex during
104 escent calcium analog terbium, we found that heparinase I tightly bound divalent and trivalent cation
105 e E2DeltaHVR1-G or E2-G pseudotypes, whereas heparinase I treatment (8 U/ml) of cells reduced 40% E2-
106 preparations of various molecular weights or heparinase I treatment of cells prevented HPV31b infecti
107 d an outer compartment where the immobilized heparinase I was fluidized separately from the blood cel
111 ations in CB-2 not only altered the kcat for heparinase I, but also resulted in incomplete degradatio
112 larly, pretreatment of eukaryotic cells with heparinase I, but not pretreatment of eukaryotic cells w
114 ective digestion with pronase, NaOH/NaBH(4), heparinase I, or low pH nitrous acid showed that each HS
115 bition of granule activity by digestion with heparinase I, the failure of proteolysis of the proteogl
116 ing studies of Woodward's reagent K-modified heparinase I, we identified two putative calcium-binding
117 d GAGs examined were effective inhibitors of heparinase I, with IC(50) values ranging from approximat
118 ide evidence that one of the active sites is heparinase I-like, cleaving at hexosamine-sulfated iduro
133 ned in the heparin binding site) inactivated heparinase I; however, a H203D mutant retained marginal
134 hexasaccharide model compounds, we show that heparinases I and II, but not heparinase III, cleave the
137 to venular endothelial cells; treatment with heparinases I and III significantly reduced this binding
138 Treatment with keratanase (3 joints) or heparinases I, II and III (3 joints) caused no significa
141 these results are due to residual HSPG since heparinase (I and III) digestion of chlorate-treated cel
144 indicating that cysteine 348 is required for heparinase II activity toward heparin but is not essenti
148 , strongly suggests that the inactivation of heparinase II by DEPC is specific for histidine residues
151 agenesis experiments on the 13 histidines of heparinase II corroborated the chemical modification and
152 n with heparan sulfate was unable to protect heparinase II from DEPC inactivation for either of the s
156 erve concentration-dependent inactivation of heparinase II in the presence of the reversible histidin
157 was found that one of the three cysteines in heparinase II is surface-accessible and possesses unusua
161 Substrate protection experiments show that heparinase II preincubation with heparin followed by the
163 cell lines with heparin, sodium chlorate, or heparinase II, demonstrating that heparin sulfate proteo
164 eparin-like glycosaminoglycan degradation by heparinase II, we set out to investigate the role of the
165 zation of heparin-like glycosaminoglycans by heparinase II, which possesses the broadest known substr
167 not cleave at GlcNH(3)(+) residues; however, heparinases II and III showed selective and distinct act
169 , removal of cell-surface heparan sulfate by heparinase III abolished the chemorepulsive response to
170 or cell treatment with chondroitinase ABC or heparinase III abolished the mitogenic effects of MK on
171 heparinase II requires O-sulfation, whereas heparinase III acts only on the corresponding non-sulfat
177 ion of heparin and the hydrolysis of HSPG by heparinase III only partially inhibited hIIA PLA2 bindin
178 Removal of the HSs from the cell surface by heparinase III or by silencing syndecan-3 by siRNA parti
180 , and pretreatment of endothelial cells with heparinase III or protease reduced dengue infectivity by
181 of heparan sulfate proteoglycans (HSPG) with heparinase III prevented infection and BM binding by the
183 fen, and enzymatic removal of HS chains with heparinase III treatment as well as by site-directed mut
188 ith a heparan sulfate antibody revealed that heparinase III treatments removed a substantial fraction
189 A(2S)-GlcNH(3)(+)(6S) disaccharides, whereas heparinase III yielded only the DeltaHexA-GlcNH(3)(+) un
190 lowing results: (1) treatment with bacterial heparinase III, an enzyme that degrades heparan sulfate
191 nsitive to digestion of cell surface HS with heparinase III, and TRSB was sensitive to both heparinas
192 was abolished after treating the cells with heparinase III, but not after chondroitinase treatment.
193 , we show that heparinases I and II, but not heparinase III, cleave the AT-III binding site, leaving
194 ate, pretreatment of conditioned medium with heparinase III, or growth of cells in sodium chlorate, i
195 by heparin and by treatment of HBEC-5i with heparinase III, suggesting that the endothelial receptor
196 cells that had been treated with the enzyme heparinase III, which degrades the glycosaminoglycan sid
198 te linkages, whereas the other is presumably heparinase III-like, cleaving at hexosamine-glucuronate
206 ndothelial cells, and binding was blocked by heparinase, indicating that secretoneurin stimulates bin
208 availability of HSPG sites as treatment with heparinase or competitors of glycosaminoglycan chain add
210 urface GAG chains by treatment of cells with heparinase or heparitinase but not chondroitinase marked
211 ll line was also inhibited by digestion with heparinase or heparitinase but not with chondroitinase A
212 fate GAGs on keratinocytes by treatment with heparinase or heparitinase resulted in an 80-90% reducti
213 dothelial cells with chondroitinase, but not heparinase or heparitinase, diminished endothelial bindi
214 is of cell surface HSPGs with, respectively, heparinase or sodium chlorate abrogated HSC adhesion to
216 ited by either prior treatment of cells with heparinases or by HS preparations enriched in 3-OS HS.
217 cosaminoglycans in embryonic stem cells with heparinases or sodium chlorate inhibited differentiation
218 oteoglycans because treatment with chlorate, heparinase, or soluble heparin did not prevent Hep II do
221 ant NOx production that was not inhibited by heparinase pretreatment, demonstrating that the cells we
223 d plasma samples, which were pretreated with heparinase prior to analysis, had the lowest baseline HI
225 teract with a widely expressed, trypsin- and heparinase-resistant cell surface molecule and facilitat
228 tment of chondrocytes with either heparin or heparinase significantly reduced attachment to type XI c
229 eparin, heparan sulfate, sodium chlorate and heparinase, the low-density lipoprotein (LDL) receptor-r
230 L1 to diminish its intravascular function or heparinase to release CXCL1 from endothelial proteoglyca
231 cetic anhydride-d6 is followed by exhaustive heparinase treatment and disaccharide analysis by hydrop
233 of 125I-bFGF to K562 cells was sensitive to heparinase treatment but not to chondroitinase treatment
234 and nonrheumatoid synovia was determined by heparinase treatment followed by an in situ binding assa
235 on assay demonstrated that entry blockage by heparinase treatment included the membrane fusion step.
242 ce heparin-like glycosaminoglycans using the heparinases, we recently have elaborated a mass spectrom
245 in (LRP), but were almost totally blocked by heparinase, which removes the sulfated glycosaminoglycan
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