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1 to oral eliglustat, a selective inhibitor of glucosylceramide synthase.
2 lic conversion by sphingomyelin synthase and glucosylceramide synthase.
3 argeted disruption of the Ugcg gene encoding glucosylceramide synthase.
4 quitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encod
5 yldeoxynojirimycin (NB-DNJ), an inhibitor of glucosylceramide synthase, a pivotal enzyme in the early
6 ceptor), and TNF-stimulated Gb3 synthase and glucosylceramide synthase activities but did not affect
7 0.01); both serine palmitoyltransferase and glucosylceramide synthase activities remained unaltered.
9 4'-Hydroxy-P4 and ethylenedioxy-P4 blocked glucosylceramide synthase activity at concentrations tha
10 d by fumonisin B(1) and by overexpression of glucosylceramide synthase; again implicating endogenous
12 mal developmental increases in activities of glucosylceramide synthase and cholesterol sulfotransfera
13 lamino-3-morpholino-1-propanol.HCI (PDMP), a glucosylceramide synthase and LacCer synthase (galactosy
14 lamino-3-morpholino-1-propanol.HCl (PDMP), a glucosylceramide synthase and LacCer synthase (GalT-2) i
15 pholino-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase and lactosylceramide synthase
16 a genome-wide forward screen that shows that glucosylceramide synthase and other components of the ga
17 ol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous
19 ed the glycosphingolipid biosynthesis enzyme glucosylceramide synthase as a direct transcriptional LX
21 d-t-EtDO-P4 has the advantage of blocking glucosylceramide synthase at low nanomolar concentration
22 Our results suggest that (a) inhibition of glucosylceramide synthase does not reverse multidrug res
23 n treatment with brain-permeant inhibitor of glucosylceramide synthase, effects mediated via improved
25 holesterol and glycosphingolipids, including glucosylceramide synthase (GCS) (gene Ugcg)-derived gang
26 n mammalian sphingomyelin synthase (SMS) and glucosylceramide synthase (GCS) and yeast inositol phosp
28 c:ceramide glucosyltransferase (EC 2.4.1.80; glucosylceramide synthase (GCS) from a rat liver and pre
35 golipid metabolism pathway via inhibition of glucosylceramide synthase (GCS) using a CNS-penetrant sm
38 native approach that involves suppression of glucosylceramide synthase (GCS), an enzyme that glycosyl
39 other glucosylceramide metabolizing enzymes, glucosylceramide synthase (GCS), lysosomal glucosylceram
41 with BFT in the presence of an inhibitor of glucosylceramide synthase (GCS), the enzyme responsible
43 s was achieved by cellular transfection with glucosylceramide synthase (GCS), the enzyme that convert
46 tiviral effect of two specific inhibitors of glucosylceramide synthase (GCS): (i) Genz-123346, an ana
49 olipid C9-methyltransferases (SmtA/SmtB) and glucosylceramide synthase (GcsA) to fungal phenotypes, s
50 n CD4(+) T cells using a potent inhibitor of glucosylceramide synthase (Genz-122346) led to a moderat
51 hibiting glycolipid biosynthesis by blocking glucosylceramide synthase has been proposed to reverse d
55 work delineates both the mechanism by which glucosylceramide synthase inhibition prevents autophagic
58 Here we show that oral administration of a glucosylceramide synthase inhibitor (GCSi) reduces plasm
59 e induction of T-cell apoptosis, because the glucosylceramide synthase inhibitor (PPPP) significantly
60 ceramide synthase inhibitor fumonisin B1 or glucosylceramide synthase inhibitor 1-phenyl-2-decanoyla
61 D4 and various chemokine receptors, with the glucosylceramide synthase inhibitor 1-phenyl-2-hexadecan
62 yristoylphosphatidylcholine liposome and the glucosylceramide synthase inhibitor D-PDMP induced cell
67 earlier studies utilized a first generation glucosylceramide synthase inhibitor to deplete cells of
68 stat is an investigational, brain-penetrant, glucosylceramide synthase inhibitor with potential to im
69 ssion was reduced approximately 40% with the glucosylceramide synthase inhibitor, d-threo-1-phenyl-2-
71 lioside synthesis in SK-RC-45 cells with the glucosylceramide synthase inhibitor, PPPP, protected T c
72 a U.S. Food and Drug Administration-approved glucosylceramide synthase inhibitor, reduced osteoclast-
73 lene, antagonists of Ryrs and by Genz-161, a glucosylceramide synthase inhibitor, suggesting substrat
74 ), proteases (trypsin and chymotrypsin), and glucosylceramide synthase inhibitors (dl-threo-1-phenyl-
76 both multidrug-resistant cell lines with the glucosylceramide synthase inhibitors PDMP (d-threo-1-phe
77 rs C9DGJ and C4DGJ, which are more selective glucosylceramide synthase inhibitors than PDMP, failed t
82 3-morpholino-1-propanol HCl, an inhibitor of glucosylceramide synthase, markedly abrogated gangliosid
83 irimycin derivatives on their merits as dual glucosylceramide synthase/neutral glucosylceramidase inh
84 xample, either ganglioside addition or human glucosylceramide synthase overexpression suppresses insu
87 Brain-permeant small-molecule inhibitor of glucosylceramide synthase reduced the accumulation of bi
88 hreo-ethylenedioxyphenyl-P4, an inhibitor of glucosylceramide synthase, restored cholesterol in cultu
89 dentified sites of action: the inhibition of glucosylceramide synthase, resulting in the depletion of
90 A null mutation of the FgGCS1 gene encoding glucosylceramide synthase results in a mutant lacking gl
91 of knockout mice with a potent inhibitor of glucosylceramide synthase reversed accumulation of globo
94 s are considerably more potent inhibitors of glucosylceramide synthase than their aliphatic counterpa
95 s led to the identification of inhibitors of glucosylceramide synthase, the enzyme catalyzing the fir
96 ted for 7 weeks with a specific inhibitor of glucosylceramide synthase, the initial enzyme involved i
97 lts provide proof of principle for targeting glucosylceramide synthase to decrease gangliosides as a
99 D-threo-3', 4'-Ethylenedioxy-P4-inhibited glucosylceramide synthase was comparably active to the p
100 the potency of these inhibitors in blocking glucosylceramide synthase was primarily dependent upon t
103 ecanoylamino-3 -pyrrolidino-1-propanol-HC l (glucosylceramide synthase), which depletes cellular gang
104 Finally, stable overexpression of human glucosylceramide synthase, which attenuates ceramide lev
105 tat, a small iminosugar, reversibly inhibits glucosylceramide synthase, which catalyses the first com
106 ort that ceramide glycosylation catalyzed by glucosylceramide synthase, which is enhanced in breast c