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1 sulfate, but it is a preferred substrate for beta-hexosaminidase.
2 oinositide (PI) hydrolysis, and secretion of beta-hexosaminidase.
3 related with release of the soluble mediator beta-hexosaminidase.
4 signal transduction defined by exocytosis of beta-hexosaminidase.
5 ce of endosomal/lysosomal markers LAMP-1 and beta-hexosaminidase.
6 ed have belonged to the large GH20 family of beta-hexosaminidases.
7 ocyclitols are potent inhibitors of N-acetyl-beta-hexosaminidases.
8 unit for the heterodimeric lysosomal enzyme, beta-hexosaminidase A (alpha beta), as well as for the h
9                                              beta-Hexosaminidase A (alphabeta) is a heterodimer, wher
10 2 in the brain, is caused by a deficiency of beta-hexosaminidase A (Hex A) or GM2 activator.
11 The catabolism of GM2 to GM3 in man requires beta-hexosaminidase A (HexA) and a protein cofactor, the
12               Loss of function of the enzyme beta-hexosaminidase A (HexA) causes the lysosomal storag
13 o participate in the formation of functional beta-hexosaminidase A activity as indicated by activator
14 enerative disorder caused by a deficiency of beta-hexosaminidase A activity.
15 lbeta1-->4Glcbet a1-1'Cer) are refractory to beta-hexosaminidase A and sialidase, respectively, we ha
16 e Neu5Ac of 6'GM2 were readily hydrolyzed by beta-hexosaminidase A and sialidase, respectively, witho
17 opes showed significant co-localization with beta-hexosaminidase A and the azurophilic marker MPO in
18          The ganglioside GM2 is processed by beta-hexosaminidase A and when non-functional GM2 accumu
19 e is responsible for the metabolic bypass of beta-hexosaminidase A deficiency.
20 expressed human azurophilic granule-resident beta-hexosaminidase A displayed the capacity to generate
21 mbranes and presents them in soluble form to beta-hexosaminidase A for cleavage of N-acetyl-d-galacto
22 activity comparable with that of recombinant beta-hexosaminidase A formed by the co-expression of the
23 wever, various strategies aimed at restoring beta-hexosaminidase A have been explored.
24 iency prevents the formation of a functional beta-hexosaminidase A heterodimer resulting in the sever
25  secreted high levels of biologically active beta-hexosaminidase A in vitro and cross-corrected the m
26                   Among human isozymes, only beta-hexosaminidase A together with the GM2 activator pr
27 he substrate (GM2) for the defective enzyme (beta-hexosaminidase A) prevents GSL accumulation and the
28 rotein to stimulate the hydrolysis of GM2 by beta-hexosaminidase A, GM2 activator was found to bind a
29 ge diseases that are caused by deficiency of beta-hexosaminidase A, which comprises an alphabeta hete
30  function in the GM2-hydrolyzing activity of beta-hexosaminidase A.
31 but not the hydrolysis of GalNAc from GM2 by beta-hexosaminidase A.
32 ytic conversion of ganglioside GM2 to GM3 by beta-hexosaminidase A.
33 he oligosaccharide from GM2 was resistant to beta-hexosaminidase A.
34 nes (HEXA and HEXB) encoding the subunits of beta-hexosaminidase A.
35                              Accumulation of beta-hexosaminidases A and B substrates is presumed to c
36                                We identified beta-hexosaminidase, a conserved enzyme across commensal
37  cells, where it reduced heparan sulfate and beta-hexosaminidase accumulation to control levels.
38  form is indicative of the action of a novel beta-hexosaminidase activity and suggests a modification
39 ge disorders characterized by the absence of beta-hexosaminidase activity and the accumulation of GM2
40 r glycolipid storage and increased levels of beta-hexosaminidase activity in visceral organs.
41 onal populations, histochemical staining for beta-hexosaminidase activity, a lysosomal enzyme involve
42 nstrated that it cosedimented with lysosomal beta-hexosaminidase activity.
43 ed ecotropic retroviruses encoding the human beta-hexosaminidase alpha-subunit cDNA and transduced mu
44                                   In humans, beta-hexosaminidase alpha-subunit deficiency prevents th
45 plant, produced substantial amounts of human beta-hexosaminidase alpha-subunit transcript and protein
46 oles were exocytic and mediated secretion of beta-hexosaminidase and cytokines accompanied by Munc13-
47 tent inhibitor than luteolin or cromolyn for beta-hexosaminidase and histamine secretion from LAD2 ce
48 age disorder characterized by the absence of beta-hexosaminidase and storage of G(M2) ganglioside and
49 yt VII inhibit Ca(2+)-triggered secretion of beta-hexosaminidase and surface translocation of Lgp120,
50 lycosaminoglycans are crucial substrates for beta-hexosaminidase and that their lack of storage in Ta
51 MMCs) from SLP76(-/-) mice failed to release beta-hexosaminidase and to secrete IL-6 after FcepsilonR
52 last-derived membranes (FBM) was measured by beta-hexosaminidase and tryptase release.
53  hydrolases, e.g., of beta-galactosidase and beta-hexosaminidases, and of GM2-activator protein, caus
54  of these enzymes, suggesting that HYAL1 and beta-hexosaminidase are functionally redundant in HA and
55                                The lysosomal beta-hexosaminidases are dimers composed of alpha and be
56 release of the secretory granule constituent beta-hexosaminidase, as well as the generation of the me
57  (alpha beta), as well as for the homodimers beta-hexosaminidase B (beta beta) and S (alpha alpha).
58 generation of lysosomal iGb3 in mice lacking beta-hexosaminidase b results in severe NKT cell deficie
59 ane, was used to identify the active site of beta-hexosaminidase B, a beta-subunit dimer.
60 t for the intimate involvement of Glu-355 in beta-hexosaminidase B-mediated catalysis.
61              We hypothesized that increasing beta-hexosaminidase (beta-hex) activity would lead to a
62  extracellular appearance of cathepsin B and beta-hexosaminidase but not cathepsins D or L.
63 a/alpha)(8) barrel topology similar to other beta-hexosaminidases but significant differences exist i
64             We have shown that expression of beta-hexosaminidase by intracranial delivery of recombin
65 ssed in vitro by using functional bioassays (beta-hexosaminidase, calcium flux, and chemokine synthes
66 ium levels in monocytes induced secretion of beta-hexosaminidase, cathepsins, and myeloperoxidase in
67 rovides in vivo evidence that both HYAL1 and beta-hexosaminidase cleave chondroitin sulfate, but it i
68 is an autosomal recessive disorder caused by beta-hexosaminidase deficiency in which the ganglioside
69 ice deficient in both enzymes, as well as in beta-hexosaminidase-deficient mice, indicating that both
70 gene signatures, improves behavior, restores beta-hexosaminidase enzymatic activity and Hexb expressi
71 d by a deficiency in the beta subunit of the beta-hexosaminidase enzyme (Hexb).
72 eases is due to functional redundancy in the beta-hexosaminidase enzyme system.
73                            The importance of beta-hexosaminidase for restricting mycobacterial growth
74 naphylactic release of renin, histamine, and beta-hexosaminidase from mast cells was confirmed in the
75 1 microM when evaluated against the N-acetyl-beta-hexosaminidase from Streptomyces plicatus.
76 d was prevented by rAAV-mediated transfer of beta-hexosaminidase gene function at considerable distan
77 o injected HDAd encoding the beta subunit of beta-hexosaminidase (Hexb) into Hexb-deficient mice, a m
78 dose- and time-regulated process that blocks beta-hexosaminidase, impacting membrane and cytoskeletal
79 y tmIgE has been confirmed by the release of beta-hexosaminidase in a cell-to-cell contact assay usin
80 one marrow mast cells blocked the release of beta-hexosaminidase in an Ag-specific fashion and preven
81 scoring the critical role of myeloid-derived beta-hexosaminidase in maintaining neuronal health and e
82 normalization of brain glycosaminoglycan and beta-hexosaminidase in MPS I mice 5 mo after moderate ye
83                      Neonatal restitution of beta-hexosaminidase in mutant mice by gene therapy succe
84 bsence of Hexb, encoding the beta subunit of beta-hexosaminidase, in both mice and patients with neur
85 a total deficiency of all forms of lysosomal beta-hexosaminidase including the small amount of beta-h
86 pharmacologic agents inhibited exocytosis of beta-hexosaminidase induced by SCF or cross-linked IgE.
87 cellular staining pattern and the release of beta-hexosaminidase into the cytosol, apoE4-transfected
88 d in neuronal homeostasis, here we show that beta-hexosaminidase is secreted by microglia and integra
89 GM2 gangliosidosis caused by a deficiency in beta-hexosaminidase, is characterized by progressive neu
90 o-tau-like immunoreactivity in the brains of beta-hexosaminidase knock-out (HEXB KO) mice.
91 infections was confirmed in macrophages from beta-hexosaminidase knockout mice.
92 umber of secondary accumulations in neurons [beta-hexosaminidase, LAMP1(lysosome-associated membrane
93 ively sensitized mice, resulted in increased beta-hexosaminidase levels in serum and BAL compared to
94                    NSCs also increased brain beta-hexosaminidase levels, reduced ganglioside storage
95 EB activation also rescues the activity of a beta-hexosaminidase mutant associated with the developme
96 ellular chitinase, a specific chitoporin, or beta-hexosaminidases, nor did they exhibit chemotaxis, t
97 elop new potent inhibitors of human N-acetyl-beta-hexosaminidases, particularly when combined with th
98 g and flow cytometry; function by release of beta-hexosaminidase, PGD(2), leukotriene C(4) (LTC(4)),
99               Histological analysis revealed beta-hexosaminidase-positive cells in the central nervou
100  the generated libraries with human N-acetyl-beta-hexosaminidases produced only moderate inhibitory a
101                                   Release of beta-hexosaminidase, prostaglandin D2, and GM-CSF and ch
102 kinase (PTK) phosphorylation, Ca++ flux, and beta-hexosaminidase release (i.e., degranulation).
103 ead, a transient attenuation of IgE-mediated beta-hexosaminidase release and cytokine production was
104 ionomycin-induced degranulation, as shown by beta-hexosaminidase release assays.
105             The mutant proteins induced less beta-hexosaminidase release from mast cells than the wil
106                      AM induced histamine or beta-hexosaminidase release from rat and human MCs throu
107 fic IgE antibodies was assessed by measuring beta-hexosaminidase release from rat basophilic leukaemi
108 hibitor LY294002, reduced agonist-stimulated beta-hexosaminidase release in a dose-dependent manner.
109 y human IgE and antigens, as demonstrated by beta-hexosaminidase release in vitro and passive cutaneo
110  by the requirement of the FYB SH3 domain in beta-hexosaminidase release, but not adhesion, and the u
111 ly, that irradiation did not directly induce beta-hexosaminidase release.
112 d by Fc gammaRII/III was not associated with beta-hexosaminidase release.
113  heritable deficiency of a lysosomal enzyme, beta-hexosaminidase, results in the storage of the enzym
114 hexosaminidase including the small amount of beta-hexosaminidase S present in the Sandhoff disease mo
115 macrophages by 100 nM C3a, (b) inhibition of beta-hexosaminidase secretion (IC(50) 8 nM) from human L
116  histamine inhibited carbachol (CCh)-induced beta-hexosaminidase secretion and prevented the formatio
117        Histamine and 5-HT acutely stimulated beta-hexosaminidase secretion at lower, but not higher,
118 t as illustrated by its ability to stimulate beta-hexosaminidase secretion from primary rabbit lacrim
119                            Net and vectorial beta-hexosaminidase secretion, cytosolic Ca(2+) (Ca(i))
120 and dose-dependent reductions of CCh-induced beta-hexosaminidase secretion.
121                 In a mouse model of colitis, beta-hexosaminidase-specific lymphocytes protected again
122 l glycosphingolipid biosynthesis inhibitors (beta-hexosaminidase substrate inhibitors) were combined
123 nt adeno-associated viral vectors expressing beta-hexosaminidase subunits (rAAV2/1-Hex).
124         To identify the domains of the human beta-hexosaminidase subunits that determine substrate sp
125  We confirm that Lyn(-/-) BMMCs release more beta-hexosaminidase than wild-type BMMCs following Fceps
126 easuring the release of the lysosomal enzyme beta-hexosaminidase, the appearance on the plasma membra
127 asis, microglia deliver the lysosomal enzyme beta-hexosaminidase to neurons for the degradation of th
128 endoglycosidase HYAL1 and the exoglycosidase beta-hexosaminidase to the lysosomal degradation of HA.
129 Ala)), were unable to target cathepsin D and beta-hexosaminidase to the lysosome.
130                                              Beta-hexosaminidase was characterized as a peptidoglycan
131 ined by RNAi depletion, the lysosomal enzyme beta-hexosaminidase was identified as an important facto
132 mulated by IgE cross-linking, the release of beta-hexosaminidase was reduced to about 20% by CE.
133 tered, widespread and abundant expression of beta-hexosaminidase with consequent clearance of glycoco

 
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