ライフサイエンスコーパス: glucosylceramide

1 ealed that virulence requires the glycolipid glucosylceramide.

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

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

4 eramide synthase results in a mutant lacking glucosylceramide.

5 the enzyme responsible for the catabolism of glucosylceramide.

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

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

8 tant cancer cells display elevated levels of glucosylceramide.

9 tant cancer cells display elevated levels of glucosylceramide.

10 H:OVCAR-3) also contained elevated levels of glucosylceramide.

11 y the plasma membrane localized sphingolipid glucosylceramide.

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

13 ctivated macrophages engorged with lysosomal glucosylceramide.

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

15 , thus designating the accumulated lipids as glucosylceramides.

16 mmediate precursor, as well as ceramides and glucosylceramides.

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

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

19 Glucosylceramides, a major component of lamellar granule

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

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

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

23 ay and enhanced expression of the endogenous glucosylceramide Ag.

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

25 Glucosylceramide also accumulated in KB-V-1, a vinblasti

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

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

28 t cleaves the O-beta-D-glucosidic linkage of glucosylceramide and aryl-beta-glucosides.

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

30 The glucosylceramide and ganglioside content of MEB4 cells e

31 In contrast to glucosylceramide and gangliosides, alterations in comple

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

33 Glucosylceramide and glucosylsphingosine accumulation in

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

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

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

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

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

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

40 The levels of glucosylceramide and lactosylceramide increased in paral

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

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

43 We found that ceramide is metabolized to glucosylceramide and sphingomyelin as it passes through

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

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

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

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

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

49 , is enriched in a more polar mixture; i.e., glucosylceramides and phospholipids, which it delivers t

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

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

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

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

54 It is concluded that high cellular levels of glucosylceramide are correlated with MDR, and that glyco

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

56 Because glucosylceramides are one of the most important lipid co

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

58 Glucosylceramide-based glycosphingolipids have been prev

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

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

61 A role for glucosylceramide-based glycosphingolipids in phospholipa

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

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

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

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

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

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

68 an essential co-factor for the hydrolysis of glucosylceramide by acid beta-glucosidase in mammals.

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

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

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

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

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

74 AdrR), which exhibits marked accumulation of glucosylceramide compared with the parental MCF-7 wild t

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

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

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

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

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

80 Since the rate of glucosylceramide degradation in MCF-7-AdrR cells was not

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

82 cerebrosidase resulting in the impairment of glucosylceramide degradation.

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

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

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

86 Glucosylceramide-depleted cells resisted treatment with

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

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

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

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

91 Incubation of cells with ceramide and glucosylceramide did not significantly stimulate p44MAPK

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

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

94 65 by controlling the UGCG-mediated ceramide/glucosylceramide equilibrium as a downstream molecular s

95 n (1:10 molar ratio with ceramide) inhibited glucosylceramide formation by nearly 50%.

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

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

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

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

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

101 Levels of ceramide, glucosylceramide, galactocerebroside, lactosylceramide,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids s

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

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

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

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

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

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

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

131 Glucosylceramide (GlcCer), one of the simplest glycosphi

132 Glucosylceramide (GlcCer), the GCase substrate, directly

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

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

135 They are derived from glucosylceramides (GlcCer) upon their extrusion from lam

136 Glucosylceramides (GlcCer), glucose-conjugated sphingoli

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Glucosylceramide is the precursor for all of the more co

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

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

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

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

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

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

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

162 Glucosylceramide levels declined after treatment of MCF-

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

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

165 all circumventors of MDR, markedly decrease glucosylceramide levels in MCF-7-AdrR cells (IC50 values

166 Antiapoptotic glucosylceramide levels were significantly increased aft

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

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

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

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

171 lucosylceramide, consistent with rapid renal glucosylceramide metabolism.

172 cellular drug resistance and alterations in glucosylceramide metabolism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 Glucosylceramide synthase (GCS) catalyzes the transfer o

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

191 Glucosylceramide synthase (GCS) inhibitors, including th

192 32 (EXEL-0346) represents a new class of glucosylceramide synthase (GCS) inhibitors.

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

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

195 Glucosylceramide synthase (GCS) transfers glucose from U

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

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

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

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

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

201 Glucosylceramide synthase (GCS), the enzyme responsible

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

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

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

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

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

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

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

209 0.01); both serine palmitoyltransferase and glucosylceramide synthase activities remained unaltered.

210 Because both sphingomyelin synthase and glucosylceramide synthase activities were significantly

211 4'-Hydroxy-P4 and ethylenedioxy-P4 blocked glucosylceramide synthase activity at concentrations tha

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

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

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

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

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

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

218 D-PDMP is a potent inhibitor of glucosylceramide synthase and thereby the synthesis of c

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

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

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

222 Conversely, silencing glucosylceramide synthase expression disrupts Gb3 synthe

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

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

225 3) Overexpression of glucosylceramide synthase in myotubes induces glucosylce

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

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

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

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

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

231 The glucosylceramide synthase inhibitor ethylenedioxyphenyl-

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

233 ssion was reduced approximately 40% with the glucosylceramide synthase inhibitor, d-threo-1-phenyl-2-

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

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

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

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

238 A new series of glucosylceramide synthase inhibitors based on substituti

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

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

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

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

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

244 iprocally modulated by chronic palmitate and glucosylceramide synthase overexpression.

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

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

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

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

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

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

251 pholino-1-propanol (D-PDMP) (an inhibitor of glucosylceramide synthase) were reduced by >90%.

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

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

254 3-morpholino-1-propanol HCl, an inhibitor of glucosylceramide synthase, markedly abrogated gangliosid

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

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

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

258 Inhibitors of glucosylceramide synthase, sphingomyelin synthase, and c

259 In cell-free assays for glucosylceramide synthase, tamoxifen (1:10 molar ratio w

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

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

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

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

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

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

266 argeted disruption of the Ugcg gene encoding glucosylceramide synthase.

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

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

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

270 Inhibition of glucosylceramide synthesis accelerated disease course in

271 In cell cultures, inhibition of glucosylceramide synthesis by tamoxifen is correlated wi

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

273 An inhibitor of glucosylceramide synthesis, 1-phenyl-2-palmitoylamino-3-

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

275 ino-3-morpholino-1-propanol, an inhibitor of glucosylceramide synthesis, likewise sensitized MCF-7-Ad

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

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

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

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

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

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

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

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

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

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

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

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

288 Whereas the extracellular processing of glucosylceramides to ceramides has been shown to be requ

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

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

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

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

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

294 Incorporation of [3H]palmitic acid into glucosylceramide was strikingly higher (8-10 times) in M

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