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1 tein LIMP-2 is a specific binding partner of beta-glucocerebrosidase.
2 osphate-independent trafficking receptor for beta-glucocerebrosidase.
3 ensitive essential, lipid-processing enzyme, beta-glucocerebrosidase.
4 lamellar membranes and decreased activity of beta-glucocerebrosidase.
5 ivation of a pH-dependent hydrolytic enzyme, beta-glucocerebrosidase.
6 cerebrosidase, which increases the levels of beta-glucocerebrosidase.
7 olding and aggregation of immature lysosomal beta-glucocerebrosidase.
8           Finally, the activity of epidermal beta-glucocerebrosidase, a key lipid-processing enzyme,
9                                              beta-glucocerebrosidase activity and protein levels were
10 y available methodologies for measuring acid beta-glucocerebrosidase activity are primarily conducted
11           Concurrently, there was diminished beta-glucocerebrosidase activity at the stratum granulos
12                     Twenty minutes postdose, beta-glucocerebrosidase activity increased over endogeno
13                                         Acid beta-glucocerebrosidase activity is measured in molecule
14  barrier recovery, attributable to decreased beta-glucocerebrosidase activity, assessed zymographical
15                                 By contrast, beta-glucocerebrosidase activity, which is responsible f
16 ellar membranes attributable to an increased beta-glucocerebrosidase activity.
17 c pH-dependent, ceramide-generating enzymes, beta-glucocerebrosidase and acidic sphingomyelinase, lea
18  assayed as inhibitor of the human lysosomal beta-glucocerebrosidase and as pharmacological chaperone
19                                Activities of beta-glucocerebrosidase and steroid sulfatase, enzymes p
20  the activity of the lipid synthetic enzymes beta-glucocerebrosidase and steroid sulfatase, markers o
21 nzymes critical to stratum corneum function, beta-glucocerebrosidase and steroid sulfatase.
22  independent lysosomal targeting, binding to beta-glucocerebrosidase (beta-GCase) and directing it to
23 rmalities were attributable to a decrease in beta-glucocerebrosidase (beta-GlcCer'ase) and acidic sph
24 pression of the key lipid processing enzyme, beta-glucocerebrosidase (beta-GlcCer'ase), develops simi
25 ression also led to lysosomal transport of a beta-glucocerebrosidase endoplasmic reticulum retention
26 tion, motor exam score, sex, depression, and beta-glucocerebrosidase (GBA) mutation status were inclu
27 ylceramide catalyzed by the lysosomal enzyme beta-glucocerebrosidase (GBA).
28 of LSDs caused by mutations to the lysosomal beta-glucocerebrosidase (GBA).
29                                              beta-Glucocerebrosidase (GBA/GCase) mutations leading to
30 n genetic disease caused by mutations in the beta-glucocerebrosidase (GBA1) gene that have been also
31                        Mutations in the acid beta-glucocerebrosidase (GBA1) gene, responsible for the
32        Mutations within the lysosomal enzyme beta-glucocerebrosidase (GC) result in Gaucher disease a
33 P-2) plays a pivotal role in the delivery of beta-glucocerebrosidase (GC) to lysosomes.
34  GBA1 gene, which result in deficient enzyme beta-glucocerebrosidase (GCase) activity and production
35 oss of activity of the lysosomal glycosidase beta-glucocerebrosidase (GCase) causes the lysosomal sto
36 ease (GD) results from mutations in the acid beta-glucocerebrosidase (GCase) encoding gene, GBA, whic
37  storage disorder caused by mutations in the beta-glucocerebrosidase (GCase) GBA gene, which result i
38 illustrate this mechanism in a case study of beta-Glucocerebrosidase (GCase) in which a vast majority
39                                              beta-Glucocerebrosidase (GCase) mutations lead to glucos
40 ions in the GBA1 gene that encodes lysosomal beta-glucocerebrosidase (GCase) represent an important r
41            Stabilization of misfolded mutant beta-glucocerebrosidase (GCase) represents an important
42 ne of the few known exceptions is the enzyme beta-glucocerebrosidase (GCase) that requires the lysoso
43 ion in male tauopathy attenuates activity of beta-glucocerebrosidase (GCase), a protein previously as
44 t (MT) alleles of the GBA1 gene that encodes beta-glucocerebrosidase (GCase), an enzyme normally traf
45 en GBA1, the gene that encodes for lysosomal beta-glucocerebrosidase (GCase), and Parkinson's disease
46 lic mutations in GBA1, the gene that encodes beta-glucocerebrosidase (GCase), cause Gaucher disease (
47 gene, which encodes for the lysosomal enzyme beta-glucocerebrosidase (GCase), resulting in the accumu
48 GBA1, the gene encoding the lysosomal enzyme beta-glucocerebrosidase (GCase), which cause Gaucher's d
49 lysosomal disease caused by mutations in the beta-glucocerebrosidase gene ( GBA1 and GCase) that have
50  hypothesized that specific mutations in the beta-glucocerebrosidase gene (GBA) causing neuropathic G
51 ive disorder caused by mutations in the acid beta-glucocerebrosidase gene.
52                               Lysosomal acid beta-glucocerebrosidase hydrolyzes glucocerebroside to g
53 Following infusion of recombinant human acid beta-glucocerebrosidase in mice, nonparenchymal cells ar
54                                  Activity of beta-glucocerebrosidase increased after PPARalpha-activa
55      Application to conduritol B epoxide-, a beta-glucocerebrosidase inhibitor, treated RAW 264.7 cel
56 ential binding among the different series of beta-glucocerebrosidase inhibitors.
57                                              Beta-glucocerebrosidase is a lysosomal hydrolase, encode
58         Carrying a variation in the gene for beta-glucocerebrosidase is a major risk factor for Parki
59 lacental-derived or recombinant form of acid beta-glucocerebrosidase is targeted to the macrophages.
60 P-2-deficient fibroblasts led to a rescue of beta-glucocerebrosidase levels and distribution.
61 arkinson disease dementia (PDD), and raising beta-glucocerebrosidase levels lowers alpha-synuclein in
62                                    Mean (SD) beta-glucocerebrosidase levels were higher at week 26 (a
63 of CSF proteins such as the lysosomal enzyme beta-glucocerebrosidase may assist in prognostication or
64 eled human placental-derived and recombinant beta-glucocerebrosidase (pGCR and rGCR, respectively).
65 ing transferrin receptor-binding moieties to beta-glucocerebrosidase (referred to as GCase-BS).
66 ity to evaluate the efficacy of in vivo acid beta-glucocerebrosidase replacement therapy in animal mo
67 cement of ER proteostasis machinery promotes beta-glucocerebrosidase solubility, while simultaneous e
68                                              beta-glucocerebrosidase, the enzyme defective in Gaucher
69                               They show that beta-glucocerebrosidase-the lysosomal enzyme defective i
70                                Missorting of beta-glucocerebrosidase was also evident in vivo, as pro
71 om these mice indicated that the majority of beta-glucocerebrosidase was secreted.
72 stingly, activity of the GBA-encoded enzyme, beta-glucocerebrosidase, was increased, suggesting the e
73 sential for normal stratum corneum function, beta-glucocerebrosidase, which converts glucosylceramide
74                  Ambroxol is a chaperone for beta-glucocerebrosidase, which increases the levels of b
75 e found to be good inhibitors of recombinant beta-glucocerebrosidase with Ki values between 8.3 and 1