ライフサイエンスコーパス: glucosylceramide

1 ctivated macrophages engorged with lysosomal glucosylceramide.

2 ealed that virulence requires the glycolipid glucosylceramide.

3 dministration of anti-CD3 antibody plus beta-glucosylceramide.

4 ns in levels of ceramide, sphingomyelin, and glucosylceramide.

5 eramide synthase results in a mutant lacking glucosylceramide.

6 the enzyme responsible for the catabolism of glucosylceramide.

7 (GCS), the enzyme that converts ceramide to glucosylceramide.

8 tant cancer cells display elevated levels of glucosylceramide.

9 hality of worms, in part, through modulating glucosylceramide.

10 y the plasma membrane localized sphingolipid glucosylceramide.

11 effects of MsDef1 on Ca(2+) were mediated by glucosylceramide.

12 ng gene, GBA, which leads to accumulation of glucosylceramides.

13 mmediate precursor, as well as ceramides and glucosylceramides.

14 A novel strategy for the synthesis of D,L-glucosylceramide 1, a member of the glycosphingolipid cl

15 Here, we report that beta-glucosylceramide 22:0 (betaGL1-22) and glucosylsphingosi

16 Here, we show that BFT increases levels of glucosylceramide, a vital intestinal sphingolipid, both

17 mellar-granule-associated antibody, and with glucosylceramides, a major lipid component of lamellar g

18 analyses showed varying rates of progressive glucosylceramide accumulation in visceral organs of pmut

19 With age, brains exhibit glucosylceramide accumulations colocalized with alpha-sy

20 ay and enhanced expression of the endogenous glucosylceramide Ag.

21 ng of a UDP-galactose: beta-d-galactosyl-1,4-glucosylceramide alpha-1, 3-galactosyltransferase (iGb(3

22 ase activity and protein levels, increase in glucosylceramide and alpha-synuclein levels as well as a

23 ivity leads to accumulation of its substrate glucosylceramide and alpha-synuclein.

24 l lipid content remained unchanged, but both glucosylceramide and ceramide content increased.

25 The glucosylceramide and ganglioside content of MEB4 cells e

26 In contrast to glucosylceramide and gangliosides, alterations in comple

27 cing GBA1 blocked PMA-induced degradation of glucosylceramide and generation of sphingosine, the sour

28 Glucosylceramide and glucosylsphingosine accumulation in

29 ice with the GCS inhibitor reduced levels of glucosylceramide and glucosylsphingosine in the central

30 In 8-week IFG-treated mice, the accumulated glucosylceramide and glucosylsphingosine were reduced by

31 ctivity and stored the glycolipid substrates glucosylceramide and glucosylsphingosine, demonstrating

32 al glucocerebrosidase levels, and storage of glucosylceramide and glucosylsphingosine.

33 Namely, the glycolipids alpha-glucosylceramide and isoglobotrihexosylceramide were pre

34 present study, d-t-EtDO-P4 depleted cellular glucosylceramide and lactosylceramide in cultured ECV304

35 The levels of glucosylceramide and lactosylceramide increased in paral

36 ow-density lipoprotein, Ca(2+) deposits, and glucosylceramide and lactosylceramide synthase activity.

37 reinforced by the identification of only one glucosylceramide and one galactosylceramide synthase, bo

38 PDMP used, conversion of ceramide into both glucosylceramide and sphingomyelin was inhibited.

39 carbon chain > or =C28) in both the ceramide/glucosylceramide and the free fatty-acid fractions.

40 w MSCs is associated with increased cellular glucosylceramide and up-regulation of inflammatory media

41 Marked accumulations of glucosylceramides and alpha-hydroxy ceramides were prese

42 ransferase, responsible for the synthesis of glucosylceramides and cholesterol sulfate, respectively,

43 particular, mTORC2 stimulated sphingolipid (glucosylceramide) and glycerophospholipid (cardiolipin)

44 Specific sphingolipids, such as ceramide, glucosylceramide, and ganglioside GM3, have been implica

45 It is speculated that an increase in glucosylceramide, and possibly higher-order glycosphingo

46 ng phosphatidylserine, ceramide-1-phosphate, glucosylceramide, and sulfatide, via the C1q domain in a

47 , sphingomyelins, phosphatidylethanolamines, glucosylceramides, and phospholipid ethers in infancy we

48 FA2H occurs prior to generation of ceramides/glucosylceramides; and 3) 2-hydroxyceramides/2-hydroxygl

49 of lamellar bodies into the stratum corneum, glucosylceramides are metabolized to ceramides, which co

50 -hydroxyceramide); and acylglucosylceramide, glucosylceramide-B, and glucosylceramide-D], whereas cer

51 Glucosylceramide-based glycosphingolipids have been prev

52 the activation of Src kinase by depletion of glucosylceramide-based glycosphingolipids in cultured EC

53 ceptor assay, demonstrated that depletion of glucosylceramide-based glycosphingolipids in cultured EC

54 A role for glucosylceramide-based glycosphingolipids in phospholipa

55 first glycosylation step in the synthesis of glucosylceramide-based glycosphingolipids.

56 of stimulating the activity of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase in a

57 anol (D-PDMP), an inhibitor of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase.

58 used beta-D-GalCer-deficient mice and beta-D-glucosylceramide (beta-D-GlcCer)-deficient cells to defi

59 lucosylceramide synthase in myotubes induces glucosylceramide but enhances insulin signaling.

60 uman keratinocytes with concurrent increased glucosylceramide but not sphingomyelin generation in the

61 e present study, the depletion of endogenous glucosylceramide by D-t-EtDO-P4 in cultured ECV304 cells

62 t acts as an activator for the hydrolysis of glucosylceramide by the enzyme glucocerebrosidase.

63 Glycolipids, identified as glucosylceramides by mass spectrometry, accumulated in t

64 ceramide-D], whereas ceramide 1, ceramide 3, glucosylceramide-C, and sphingomyelin remained unchanged

65 der caused by a defect in the degradation of glucosylceramide catalyzed by the lysosomal enzyme beta-

66 cerebrosidase (GBA, the enzyme that degrades glucosylceramide), colonoid permeability was reduced, an

67 (GCS), the enzyme responsible for generating glucosylceramide, colonoids become highly permeable, los

68 e biological consequences of the increase in glucosylceramide composition, R28 retinal neurons were t

69 e via fasting did not affect the increase in glucosylceramide composition.

70 t-EtDO-P4 was abolished by exogenously added glucosylceramide, consistent with a specific glycosphing

71 EtDO-P4 resulted in a 55% reduction in renal glucosylceramide, consistent with rapid renal glucosylce

72 cylglucosylceramide, glucosylceramide-B, and glucosylceramide-D], whereas ceramide 1, ceramide 3, glu

73 cerebrosidase resulting in the impairment of glucosylceramide degradation.

74 hibitor of acid beta-glucosidase, and lowers glucosylceramide degradation.

75 characterized impact of CBE on the lysosomal glucosylceramide-degrading enzyme (glucocerebrosidase, G

76 g the cell wall-associated glycosphingolipid glucosylceramide (Delta gcs1), previously characterized

77 hat a Cryptococcus neoformans mutant lacking glucosylceramide (Deltagcs1) is avirulent and unable to

78 Taken together, our data demonstrate a glucosylceramide-dependent mechanism by which the colon

79 Glucosylceramide-depleted cells resisted treatment with

80 C-gamma1 was enhanced by EGF stimulation in glucosylceramide-depleted cells, associated with enhance

81 lipase C-gamma1 in control cells, whereas in glucosylceramide-depleted cells, suppression of Src kina

82 ities of Src kinase were also induced in the glucosylceramide-depleted cells.

83 y promote excess accumulation of ceramide or glucosylceramide derivatives, which impair insulin actio

84 ituents in the aminocyclitols and the parent glucosylceramide does not seem to be strictly necessary

85 proportions of glycerol, Pluronic F-127, and glucosylceramide enhanced naproxen entry.

86 65 by controlling the UGCG-mediated ceramide/glucosylceramide equilibrium as a downstream molecular s

87 this enzyme, and hence for optimal levels of glucosylceramide, for efficient trafficking of endogenou

88 observed to be even more active in blocking glucosylceramide formation.

89 d the potency of these compounds in blocking glucosylceramide formation.

90 , a macrophage containing much of the stored glucosylceramide found in tissues, which is believed to

91 Synthesis of the corresponding ceramide and glucosylceramide fractions was enhanced by vitamin C, at

92 acids (mmBCFAs) and their derivative, d17iso-glucosylceramide, function in the intestine to promote f

93 Levels of ceramide, glucosylceramide, galactocerebroside, lactosylceramide,

94 und to stimulate the enzymatic hydrolysis of glucosylceramide, galactosylceramide, and sphingomyelin.

95 s, which are converted to sphingomyelins and glucosylceramides/gangliosides by the addition of polar

96 9H;C* mice developed significant visceral glucosylceramide (GC) and glucosylsphingosine (GS) accum

97 e) in Gaucher disease causes accumulation of glucosylceramide (GC) and glucosylsphingosine (GS) that

98 tem (CNS) phenotype attributed to diminished glucosylceramide (GC) cleavage activity by acid beta-glu

99 A1 mutations drive extensive accumulation of glucosylceramide (GC) in multiple innate and adaptive im

100 ) and moderate elevation (1.5- to 3-fold) of glucosylceramide (GC) were in 4L;C* brains.

101 d beta-glucosidase (GCase) and the resultant glucosylceramide (GC)/glucosylsphingosine (GS) accumulat

102 increased GCase activity, reduced substrate [glucosylceramide (GC, -34%) and glucosylsphingosine (GS,

103 s the accumulation of two key sphingolipids, glucosylceramide (GL-1) and glucosylsphingosine (LysoGL-

104 Drug treatment reduced liver glucosylceramide (GL1) levels in the ob/ob mouse.

105 Here we demonstrate that kidney glucosylceramide (GlcCer) and ganglioside GM3 levels are

106 leads to the accumulation of two substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSp

107 Specifically, we found that glucosylceramide (GlcCer) and lactosylceramide (LacCer)

108 The primary substrates of Dnf2 are glucosylceramide (GlcCer) and phosphatidylcholine (PC, o

109 the content of sphingomyelin, ceramide, and glucosylceramide (GlcCer) in circulating lipoproteins in

110 ting evidence suggests a pathogenic role for glucosylceramide (GlcCer) in multiple forms of PKD.

111 he sequential addition of monosaccharides to glucosylceramide (GlcCer) in the lumen of the Golgi appa

112 C8-desaturated and C9-methylated glucosylceramide (GlcCer) is a fungal-specific sphingoli

113 Glucosylceramide (GlcCer) is a ubiquitous glycosphingoli

114 mass of lactosylceramide and an increase in glucosylceramide (GlcCer) level.

115 Reduction in glucosylceramide (GlcCer) levels led to complete protect

116 d pathogenicity of a Cryptococcus neoformans glucosylceramide (GlcCer) mutant shines new light on the

117 The effect of glucosylceramide (GlcCer) on activated protein C (APC)-p

118 ionship between venous thrombosis and plasma glucosylceramide (GlcCer) or phosphatidylethanolamine (P

119 2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids s

120 mino-3-pyrrolidino-1-propanol (EtDO-P4), the glucosylceramide (GlcCer) synthase inhibitor, which depl

121 Recently, the fungal sphingolipid glucosylceramide (GlcCer) synthesis has emerged as a hig

122 non-lysosomal beta-glucosidase GBA2 degrade glucosylceramide (GlcCer) to glucose and ceramide in dif

123 BA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.

124 hosphate adaptor protein 2 (FAPP2) transfers glucosylceramide (GlcCer), a lipid that takes an unexpec

125 tural isolates of lactosylceramide (LacCer), glucosylceramide (GlcCer), and galactosylceramide (GalCe

126 eratinocyte differentiation, the glycolipid, glucosylceramide (GlcCer), is thought to be synthesized,

127 Glucosylceramide (GlcCer), lactosylceramide (LacCer), an

128 Glucosylceramide (GlcCer), one of the simplest glycosphi

129 Glucosylceramide (GlcCer), the GCase substrate, directly

130 Glucosylceramide (GlcCer), the initial GSL synthesized f

131 Here we show that the glycosphingolipid glucosylceramide (GlcCer), which is present in C. neofor

132 Glucosylceramides (GlcCer) and ceramides (Cer) appear to

133 Glucosylceramides (GlcCer), glucose-conjugated sphingoli

134 ges in sphingolipids including ceramides and glucosylceramides (GlcCer).

135 We have previously reported that mammalian glucosylceramides (GlcCers) activate iNKT cells.

136 y is associated with the accumulation of its glucosylceramide (GluCer) substrate in PD brain tissues.

137 nto compact, assembly-state intermediates by glucosylceramide (GluCer), without apparent disassembly

138 show that, whereas GD-related sphingolipids (glucosylceramide, glucosylsphingosine, sphingosine, sphi

139 Increased ceramide, glucosylceramide, GM3, and hexosaminidase activity were

140 e, suggesting that BFT-induced production of glucosylceramide helps to stabilize tight junctions.

141 , we found increased cholesterol and altered glucosylceramide homeostasis which could compromise ALR.

142 tagcs1, we studied the role of C. neoformans glucosylceramide in a T- and NK-cell-immunodeficient mou

143 ad little GC enzyme activity and accumulated glucosylceramide in brain and liver.

144 C activity and no detectable accumulation of glucosylceramide in brain and liver.

145 ceramide was efficiently converted to NBD C6-glucosylceramide in live cells or in mouse tissues, wher

146 a functional role of the fungal sphingolipid glucosylceramide in regulating sensitivity of the fungus

147 severe lysosomal defects and accumulation of glucosylceramide in the fly brain.

148 abled detection and quantification of NBD C6-glucosylceramide in the low-femtomolar range.

149 n progressive accumulation of the substrate (glucosylceramide) in macrophages, leading to hepatosplen

150 e examined the role of a third sphingolipid, glucosylceramide, in influenza virus infection following

151 Several of these-ceramides and glucosylceramides-induced differentiation when added to

152 is an enzyme that cleaves the membrane lipid glucosylceramide into glucose and ceramide.

153 catalyzes the cleavage of a major glycolipid glucosylceramide into glucose and ceramide.

154 Based on our findings, we conclude that glucosylceramide is essential for MsDef1-mediated growth

155 Glucosylceramide is the precursor for all of the more co

156 that an mmBCFA-derived sphingolipid, d17iso-glucosylceramide, is a critical metabolite in regulating

157 mediator ceramide to a nonfunctional moiety glucosylceramide, is overexpressed in many MDR tumor typ

158 s supplemented with ceramide, sphingomyelin, glucosylceramide, lactosylceramide, and ganglioside G(D3

159 ral blood neutrophils, myeloblasts expressed glucosylceramide, lactosylceramide, and the neolacto-fam

160 es were characterized as galactosylceramide, glucosylceramide, lactosylceramide, galabiaosylceramide,

161 te the degradation of both sphingomyelin and glucosylceramide leading to the salvage pathway of ceram

162 of these mutants revealed a 50% reduction in glucosylceramide levels and a corresponding increase in

163 Glucosylceramide levels declined after treatment of MCF-

164 By increasing glucosylceramide levels in colonoids via an inhibitor of

165 a significant approximately 30% increase in glucosylceramide levels in fed diabetic rats compared wi

166 howed a concentration-dependent decrement in glucosylceramide levels in kidney, liver, and spleen.

167 Modulation of glucosylceramide levels may therefore represent a novel

168 Antiapoptotic glucosylceramide levels were significantly increased aft

169 sociated gammopathy is reactive against lyso-glucosylceramide (LGL1), which is markedly elevated in t

170 ipids directly to the worms, we suggest that glucosylceramide may be a key mediator of the effects of

171 dy showing that modulating the catabolism of glucosylceramide may be a therapeutic target for this de

172 mal permeability barrier caused by defective glucosylceramide metabolism in the epidermis.

173 lucosylceramide, consistent with rapid renal glucosylceramide metabolism.

174 on GBA2 selectivity offset against the other glucosylceramide metabolizing enzymes, glucosylceramide

175 ytes increased significantly by 8 h, whereas glucosylceramide only modestly increased, and sphingomye

176 of lesser magnitude than those obtained with glucosylceramide or at pH 6.3.

177 tant mice do not accumulate large amounts of glucosylceramide or exhibit classic Gaucher cells in tis

178 -ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon

179 es ceramide levels by converting ceramide to glucosylceramide, prevented the inhibitory effects of C(

180 ched-chain fatty acids (mmBCFAs) and derived glucosylceramide promote intestinal TORC1 activity for p

181 ptotic metabolites such as sphingomyelin and glucosylceramide protects cells from ceramide-induced ap

182 We discuss the possible connections among glucosylceramide, protein aggregate clearance, and autop

183 either GM3, c-Src, nor Rho A but did contain glucosylceramide, Ras, a very small quantity of sphingom

184 Moreover, selected ceramide and glucosylceramide species: i.e., nonhydroxy ceramide 2 an

185 ramide (C(2)-Cer and C(6)-Cer), but not C(8)-glucosylceramides, sphingosine, or ceramide 1-phosphate,

186 spastic ataxia and responsible for a form of glucosylceramide storage disease in humans.

187 Among tested sphingolipid analogs of glucosylceramide, sulfatide, ganglioside GM1, ceramide 1

188 holesterol and glycosphingolipids, including glucosylceramide synthase (GCS) (gene Ugcg)-derived gang

189 n mammalian sphingomyelin synthase (SMS) and glucosylceramide synthase (GCS) and yeast inositol phosp

190 Glucosylceramide synthase (GCS) catalyzes the transfer o

191 Here, we investigated the merits of glucosylceramide synthase (GCS) inhibition as a potentia

192 Glucosylceramide synthase (GCS) inhibitors, including th

193 32 (EXEL-0346) represents a new class of glucosylceramide synthase (GCS) inhibitors.

194 In this study, we have introduced glucosylceramide synthase (GCS) into wild type MCF-7 bre

195 Glucosylceramide synthase (GCS) is a rate-limiting enzym

196 Glucosylceramide synthase (GCS) transfers glucose from U

197 Overexpression of glucosylceramide synthase (GCS), a pivotal enzyme in gly

198 Ceramide glycosylation, through glucosylceramide synthase (GCS), allows cellular escape

199 native approach that involves suppression of glucosylceramide synthase (GCS), an enzyme that glycosyl

200 other glucosylceramide metabolizing enzymes, glucosylceramide synthase (GCS), lysosomal glucosylceram

201 The enzyme glucosylceramide synthase (GCS), responsible for bioacti

202 with BFT in the presence of an inhibitor of glucosylceramide synthase (GCS), the enzyme responsible

203 Glucosylceramide synthase (GCS), the enzyme responsible

204 s was achieved by cellular transfection with glucosylceramide synthase (GCS), the enzyme that convert

205 through up-regulating the gene expression of glucosylceramide synthase (GCS).

206 Since clearance is mediated by glucosylceramide synthase (GCS, EC 2.4.1.80) levels of t

207 Microarray data demonstrated that glucosylceramide synthase (GCS; glucosylceramide transfe

208 olipid C9-methyltransferases (SmtA/SmtB) and glucosylceramide synthase (GcsA) to fungal phenotypes, s

209 n CD4(+) T cells using a potent inhibitor of glucosylceramide synthase (Genz-122346) led to a moderat

210 ceptor), and TNF-stimulated Gb3 synthase and glucosylceramide synthase activities but did not affect

211 0.01); both serine palmitoyltransferase and glucosylceramide synthase activities remained unaltered.

212 Because both sphingomyelin synthase and glucosylceramide synthase activities were significantly

213 4'-Hydroxy-P4 and ethylenedioxy-P4 blocked glucosylceramide synthase activity at concentrations tha

214 ed by PDMP cannot be caused by inhibition of glucosylceramide synthase alone.

215 mal developmental increases in activities of glucosylceramide synthase and cholesterol sulfotransfera

216 lamino-3-morpholino-1-propanol.HCI (PDMP), a glucosylceramide synthase and LacCer synthase (galactosy

217 lamino-3-morpholino-1-propanol.HCl (PDMP), a glucosylceramide synthase and LacCer synthase (GalT-2) i

218 pholino-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase and lactosylceramide synthase

219 a genome-wide forward screen that shows that glucosylceramide synthase and other components of the ga

220 ol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous

221 s compound, D-threo-4'-hydroxy-P4, inhibited glucosylceramide synthase at an IC50 of 90 nM.

222 d-t-EtDO-P4 has the advantage of blocking glucosylceramide synthase at low nanomolar concentration

223 Our results suggest that (a) inhibition of glucosylceramide synthase does not reverse multidrug res

224 Conversely, silencing glucosylceramide synthase expression disrupts Gb3 synthe

225 hibiting glycolipid biosynthesis by blocking glucosylceramide synthase has been proposed to reverse d

226 hance insulin signaling, but those targeting glucosylceramide synthase have no effect.

227 3) Overexpression of glucosylceramide synthase in myotubes induces glucosylce

228 In the Zucker diabetic fatty rat, the glucosylceramide synthase inhibitor (1R,2R)-nonanoic aci

229 e induction of T-cell apoptosis, because the glucosylceramide synthase inhibitor (PPPP) significantly

230 ceramide synthase inhibitor fumonisin B1 or glucosylceramide synthase inhibitor 1-phenyl-2-decanoyla

231 D4 and various chemokine receptors, with the glucosylceramide synthase inhibitor 1-phenyl-2-hexadecan

232 yristoylphosphatidylcholine liposome and the glucosylceramide synthase inhibitor D-PDMP induced cell

233 The glucosylceramide synthase inhibitor ethylenedioxyphenyl-

234 Inhibition of GSL synthesis with the glucosylceramide synthase inhibitor Genz-667161 decrease

235 earlier studies utilized a first generation glucosylceramide synthase inhibitor to deplete cells of

236 Complications observed with another glucosylceramide synthase inhibitor, N-butyldeoxynojirim

237 lioside synthesis in SK-RC-45 cells with the glucosylceramide synthase inhibitor, PPPP, protected T c

238 lene, antagonists of Ryrs and by Genz-161, a glucosylceramide synthase inhibitor, suggesting substrat

239 ), proteases (trypsin and chymotrypsin), and glucosylceramide synthase inhibitors (dl-threo-1-phenyl-

240 A new series of glucosylceramide synthase inhibitors based on substituti

241 both multidrug-resistant cell lines with the glucosylceramide synthase inhibitors PDMP (d-threo-1-phe

242 rs C9DGJ and C4DGJ, which are more selective glucosylceramide synthase inhibitors than PDMP, failed t

243 Recently, more active and specific glucosylceramide synthase inhibitors, including d-threo-

244 ition, R28 retinal neurons were treated with glucosylceramide synthase inhibitors.

245 nant glucocerebrosidase and orally-available glucosylceramide synthase inhibitors.

246 xample, either ganglioside addition or human glucosylceramide synthase overexpression suppresses insu

247 iprocally modulated by chronic palmitate and glucosylceramide synthase overexpression.

248 A null mutation of the FgGCS1 gene encoding glucosylceramide synthase results in a mutant lacking gl

249 of knockout mice with a potent inhibitor of glucosylceramide synthase reversed accumulation of globo

250 s are considerably more potent inhibitors of glucosylceramide synthase than their aliphatic counterpa

251 We used a potent inhibitor of glucosylceramide synthase to test whether substrate depr

252 D-threo-3', 4'-Ethylenedioxy-P4-inhibited glucosylceramide synthase was comparably active to the p

253 the potency of these inhibitors in blocking glucosylceramide synthase was primarily dependent upon t

254 ecanoylamino-3 -pyrrolidino-1-propanol-HC l (glucosylceramide synthase), which depletes cellular gang

255 quitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encod

256 yldeoxynojirimycin (NB-DNJ), an inhibitor of glucosylceramide synthase, a pivotal enzyme in the early

257 3-morpholino-1-propanol HCl, an inhibitor of glucosylceramide synthase, markedly abrogated gangliosid

258 Thus, overexpression of glucosylceramide synthase, previously shown to protect a

259 hreo-ethylenedioxyphenyl-P4, an inhibitor of glucosylceramide synthase, restored cholesterol in cultu

260 dentified sites of action: the inhibition of glucosylceramide synthase, resulting in the depletion of

261 Inhibitors of glucosylceramide synthase, sphingomyelin synthase, and c

262 s led to the identification of inhibitors of glucosylceramide synthase, the enzyme catalyzing the fir

263 ted for 7 weeks with a specific inhibitor of glucosylceramide synthase, the initial enzyme involved i

264 Sphingomyelin synthase, as well as glucosylceramide synthase, was inactivated by PDT in bot

265 Finally, stable overexpression of human glucosylceramide synthase, which attenuates ceramide lev

266 tat, a small iminosugar, reversibly inhibits glucosylceramide synthase, which catalyses the first com

267 ort that ceramide glycosylation catalyzed by glucosylceramide synthase, which is enhanced in breast c

268 lic conversion by sphingomyelin synthase and glucosylceramide synthase.

269 argeted disruption of the Ugcg gene encoding glucosylceramide synthase.

270 to oral eliglustat, a selective inhibitor of glucosylceramide synthase.

271 irimycin derivatives on their merits as dual glucosylceramide synthase/neutral glucosylceramidase inh

272 d by fumonisin B(1) and by overexpression of glucosylceramide synthase; again implicating endogenous

273 Inhibition of glucosylceramide synthesis accelerated disease course in

274 sient ganglioside depletion by inhibition of glucosylceramide synthesis of MEB4 melanoma cells in vit

275 some inhibitor, bortezomib, or inhibition of glucosylceramide synthesis with eliglustat, partially co

276 orpholino-1-propanol (PPMP), an inhibitor of glucosylceramide synthesis, blocked karyokinesis and red

277 t of the host with a novel p.o. inhibitor of glucosylceramide synthesis, the imino sugar OGT2378, inh

278 We previously found that glucosylceramide, the glycosylated form of ceramide, acc

279 ion, but the addition of galactosylceramide, glucosylceramide, the monosialoganglioside, GM3, lactosy

280 glucose from UDP-glucose to ceramide to form glucosylceramide, the precursor of most higher order gly

281 ramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearanc

282 se (GBA), a lysosomal enzyme that hydrolyzes glucosylceramide to ceramide and glucose.

283 ion, beta-glucocerebrosidase, which converts glucosylceramide to ceramide, and steroid sulfatase, whi

284 cid beta-glucosidase 1 (GBA1), which cleaves glucosylceramide to ceramide.

285 beta-glucosidase 1 (GBA1), which hydrolyzes glucosylceramide to form lysosomal ceramide, was involve

286 ase beta2 (GBA2) catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.

287 rate concentration, enabling GC to hydrolyze glucosylceramide to glucose and ceramide.

288 Recombinant GBA2 hydrolyzed glucosylceramide to glucose and ceramide; the same react

289 the requirement for enzymatic hydrolysis of glucosylceramides to ceramide for epidermal barrier home

290 transporter that facilitates the delivery of glucosylceramides to epidermal lamellar bodies in kerati

291 lycosphingolipids, particularly ceramide and glucosylceramide, to neurodegeneration and to motor unit

292 strated that glucosylceramide synthase (GCS; glucosylceramide transferase), but not acid sphingomyeli

293 Here, we report that giardial glucosylceramide transferase-1 (gGlcT1), an enzyme of sp

294 lyze the crucial modification of ceramide to glucosylceramide via UDP-glucose ceramide glucosyltransf

295 The product of CGT (glucosylceramide) was also increased.

296 r lipid Ags presented by CD1d, such as alpha-glucosylceramide, was distinct from type I NKT cells.

297 orylation of Tyr-529 induced by depletion of glucosylceramide were maintained.

298 euraminosyl-alpha(2, 3)-galactosyl-beta(1,4)-glucosylceramide), were inactive in causing vesicle form

299 poorly to a glucose-linked glycolipid (alpha-glucosylceramide), which correlated with their lack of a

300 ity of Valpha24- T cells to respond to alpha-glucosylceramide, which differs from alphaGalCer in the