ライフサイエンスコーパス: ceramide

1 hese compartments and may directly transport ceramide.

2 c phenotype as did the addition of exogenous ceramide.

3 atalyzes the degradation of sphingomyelin to ceramide.

4 otic shock, bacterial sphingomyelinase or C6 ceramide.

5 erts sphingomyelin into the signaling lipid, ceramide.

6 e UPR by increasing the de novo synthesis of ceramide.

7 at least in part, mediated the action of C6-ceramide.

8 ave identified a novel antifibrotic role for ceramide.

9 d cell membrane component sphingomyelin into ceramide.

10 on of dermal cholesterol, triglycerides, and ceramides.

11 n enzyme in the de novo synthesis pathway of ceramides.

12 The highest accumulation was in hydroxy-ceramides.

13 ER prevents the buildup of toxic amounts of ceramides.

14 75 nm that are composed of at least about 20 ceramides.

15 accumulation of nonesterified omega-hydroxy-ceramides.

16 lipid transfer protein that is specific for ceramide 1-phosphate (C1P) and phyto-C1P.

17 ated the potential for another sphingolipid, ceramide 1-phosphate (C1P), to modulate efflux pumps at

18 Recently, ceramide-1-phosphate (C1P) has been shown to modulate ac

19 The C1P binding site in ACD11 and in human ceramide-1-phosphate transfer protein (CPTP) is surround

20 Ceramide, a bioactive lipid and signaling molecule assoc

21 Ceramide, a mediator of lipotoxicity, was increased in P

22 n (SM) requires its initial degradation into ceramide, a process catalyzed by the intestinal enzyme a

23 f m/z 572.48 [Cer(d34:1) + Cl](-) which is a ceramide absent from the viable cancer subregions; (2) t

24 As seen with administration of exogenous ceramide, AC ablation blocks cell cycle progression and

25 mide synthases increased enzyme activity and ceramide accumulation after IR.

26 Mitochondrial ceramide accumulation and lethal mitophagy induction in

27 emius) was analyzed for insulin sensitivity, ceramide accumulation and the post translational modific

28 2:0) similarly promotes a global increase in ceramide accumulation in human neurons which was associa

29 Mechanistically, FLT3-ITD targeting induced ceramide accumulation on the outer mitochondrial membran

30 ne inhibited acid sphingomyelinase activity, ceramide accumulation, and microparticle production duri

31 ne inhibited acid sphingomyelinase activity, ceramide accumulation, and microparticle production duri

32 ctivation, inflammatory cytokine expression, ceramide accumulation, reductions in brain volume, synap

33 Ceramides act as a double-edged sword, promoting normal

34 Recently, it has been demonstrated that the ceramide acylation pattern is of particular importance f

35 e synthesized nontoxic, azido-functionalized ceramides allowing for bio-orthogonal click-reactions to

36 ttack of a zinc-bound hydroxide ion onto the ceramide amide carbonyl.

37 ional deficiency of Fas limits both FasL and ceramide analogs in the induction of apoptosis.

38 Five ceramide analogs, IG4, IG7, IG14, IG17, and IG19, exhibi

39 oted by curcumin, a drug known to perturb ER ceramide and calcium homeostasis.

40 Since increases in ceramide and consequent decreases of S1P reduce prolifer

41 ession, resulting in further accumulation of ceramide and consequent reduction of surface sphingosine

42 in base (LCB) substrates and decrease in C18 ceramide and derivatives in the brain, leading to neurod

43 also influenced the segregation of palmitoyl ceramide and dipalmitoylglycerol into an ordered phase.

44 SORT1 deficiency did not alter hepatic ceramide and fatty acid metabolism in high cholesterol a

45 l enzyme that hydrolyzes glucosylceramide to ceramide and glucose.

46 gulation of glycosphingolipids, particularly ceramide and glucosylceramide, to neurodegeneration and

47 CerS6 preferentially generates C16-ceramide and its mRNA is highly expressed in immune tiss

48 Ceramide and more complex sphingolipids constitute a div

49 ealed that these molecules can modulate both ceramide and sphingomyelin pools in cells and inhibit ce

50 An investigation of the respective ceramide and sphingomyelin populations in L3.6pl cells r

51 tions in sphingolipid metabolism, especially ceramide and sphingosine 1-phosphate, have been linked t

52 Our results highlight an imbalance in brain ceramide and sphingosine in the early stages of neurodeg

53 biosynthesis, underscoring the importance of ceramide and sphingosine synthesis pathways in skin and

54 a1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that tr

55 n pRBCs was associated with the formation of ceramide and the release of microparticles.

56 tion of aCDase also promoted accumulation of ceramide and was associated with reduced COL1A1 expressi

57 common for all of the CerS isoforms, but not ceramides and complex sphingolipids, were restored to th

58 ngolipid signaling by lowering the levels of ceramides and concomitantly increasing those of sphingos

59 PP2A is activated by ceramides and dephosphorylates Akt.

60 investigated the association between plasma ceramides and risk of CVD.

61 imilar degree, causing accumulation of C16:0-ceramide (and some C18:0-, C20:0-, and C22:0-ceramides)

62 on of nCDase in colon cancer cells increases ceramide, and this is accompanied by decreased cell surv

63 utants also possess reduced GIPCs, increased ceramides, and an increased incorporation of short-chain

64 of triglycerides, diglycerides, fatty acids, ceramides, and oxidized fatty acids, as well as low leve

65 eactions to fluorescently label incorporated ceramides, and thus investigate formation of ceramide-en

66 Ceramides are bioactive sphingolipids, which are compose

67 c reticulum (ER) to the Golgi complex, where ceramides are converted to complex sphingolipids.

68 Ceramides are endogenous skin lipids essential for maint

69 Ceramides are key intermediates in sphingolipid biosynth

70 delian disorders of keratinization, although ceramides are known to have key roles in several biologi

71 itions and cell type 50-60 % of all membrane ceramides are located in ceramide-rich platforms (CRPs)

72 Therefore, the functionalized ceramides are novel, highly potent tools to study the su

73 Ceramides are synthesized by a family of six ceramide sy

74 Thus, ceramides are vital players in numerous diseases includi

75 Our study identified ceramide as a bioactive lipid that limits PI3KC2beta-gov

76 identified C22:1-CoA, C2-carnitine, and C16-ceramide as the best classifiers.

77 ceramide (and some C18:0-, C20:0-, and C22:0-ceramides) as well as C16:0- and C18:0-Hex-Cers.

78 rs such as sphinganine, dihydroceramide, and ceramide; (b) inhibited insulin stimulation of a central

79 findings could be translated into developing ceramide-based therapy for metastatic diseases.

80 WT)-LC3, but not mutants of LC3 with altered ceramide binding (I35A-LC3 or F52A-LC3).

81 n this structure, no FFA is observed and the ceramide binding pocket and putative zinc catalytic site

82 We also identify a ceramide binding pose and propose a possible mechanism f

83 and associated with hepatic accumulation of ceramides, bioactive lipids implicated in alcoholic live

84 IRT3 involvement in modulating mitochondrial ceramide biosynthesis and suggest an important role of S

85 Mutations in ceramide biosynthesis pathways have been implicated in a

86 we report that SIRT3 regulates mitochondrial ceramide biosynthesis via deacetylation of ceramide synt

87 Mutations in KDSR cause defective ceramide biosynthesis, underscoring the importance of ce

88 cultured myotubes, these tissues accumulated ceramides but not SMs.

89 olenopsin analogs which biochemically act as ceramides, but cannot be metabolized to S1P.

90 nversion of apical membrane sphingomyelin to ceramide by exogenous bacterial sphingomyelinase (SMase)

91 indicate that reduction of endogenous C16:0-ceramide by genetic inhibition ofCerS5is sufficient to a

92 Ceramide-C16 (CerC16) is a sphingolipid associated with

93 n, Golgi membrane lipid order disruption byd-ceramide-C6 causes Golgi pH alkalization.

94 which synthesizes 18-carbon fatty acyl (C18) ceramide, cause elevation of long-chain base (LCB) subst

95 profoundly affected, showing an increase in ceramide (Cer) and a decrease in sphingomyelin (SM) and

96 An increase of ceramide (Cer) was a hallmark for LPS activation.

97 ted FAs, induced the production of cytotoxic ceramides (Cers) in macrophage cell lines.

98 nsistent with the hypothesis of an apoptotic ceramide channel, we have used here assays of calcein re

99 quence, the hypothesis of formation of large ceramide channels in the membrane is not consistent with

100 s on the depletion of cholesterol from a C16 ceramide/cholesterol (C16-Cer/Chol) mixed monolayer usin

101 Simultaneously, the ceramide concentration in CRPs increases approximately t

102 ingomyelinase (bSMase) increases the overall ceramide concentration in the plasma membrane, the quant

103 Changes in ceramide concentration were not significantly different

104 positive association between baseline plasma ceramide concentrations and incident CVD.

105 Furthermore, SAT ceramide concentrations correlated with the expression o

106 ntial deleterious effects of elevated plasma ceramide concentrations on CVD.

107 gether with some all-or-none leakage (at low ceramide concentrations or short times).

108 Plasma ceramide concentrations were measured on a liquid chroma

109 ontent (60%, P < 0.01) but a 30% increase in ceramide content (P < 0.001).

110 ytic LPL deficiency also triggered increased ceramide content in the hypothalamus, which may contribu

111 flammasome together with the associated high ceramide content in the plasma and SAT of obese adolesce

112 is induced by both inflammation signals and ceramide, could play a major role in the development of

113 nic lipid, and treatment with short-chain C6-ceramide decreased the number of ovarian cancer cells wi

114 Inhibition of Drp1 prevented ceramide-dependent lethal mitophagy, and reconstitution

115 in crenolanib-resistant AML cells suppressed ceramide-dependent mitophagy and prevented cell death.

116 and cell size are mechanistically linked by ceramide-dependent signals arising from the TORC2 networ

117 enriched, coexisting with a Lalpha phase, or ceramide depleted, coexisting with a Lbeta phase, depend

118 s, nor were there changes in skeletal muscle ceramide, diacylglycerol, or amino acid metabolite level

119 ry revealed elevations of ceramides, hydroxy-ceramides, dihydroceramides, sphingosine, dihexosylceram

120 ure appropriately balanced nutrient sensing, ceramide distribution, body weight regulation, and gluco

121 In Caco-2/TC7 enterocytes, ceramide effects on insulin-dependent AKT phosphorylatio

122 se would be due to a competition between two ceramide effects; namely, lateral segregation that facil

123 Ceramide enhances FasL-induced activation of the MAPK, N

124 The resulting HII phase can be ceramide enriched, coexisting with a Lalpha phase, or ce

125 ceramides, and thus investigate formation of ceramide-enriched domains.

126 Ceramide-enriched exosomes appear to exacerbate AD-relat

127 of neutral sphingomyelinase-2 function, that ceramide-enriched exosomes exacerbate AD-related patholo

128 applies to T lymphocytes where formation of ceramide-enriched membrane microdomains modulates TCR si

129 Thus, cells that cannot make ceramides fail to modulate their growth rate or size in

130 re incubated with palmitate or directly with ceramide for short or long periods, and insulin signalin

131 It has been proposed that ceramide forms large and stable channels in the mitochon

132 gomyelin requires non-vesicular transport of ceramide from the endoplasmic reticulum to the Golgi by

133 Nvj2p promotes the nonvesicular transfer of ceramides from the ER to the Golgi complex.

134 lts demonstrate that the DK switch regulates ceramide generation by nSMase2 and is governed by an all

135 Here, we reveal that pro-cell death lipid ceramide generation is suppressed by FLT3-ITD signaling.

136 oduct of the SMPD3 gene) is a key enzyme for ceramide generation that is involved in regulating cellu

137 y in a mouse model with consistently reduced ceramide generation.

138 of retinoic acid on alternative pathways for ceramide generation.

139 ase (MGAT1) and GSLs by deleting UDP-glucose ceramide glucosyltransferase (UGCG).

140 the key GSL biosynthetic enzyme UDP-glucose ceramide glucosyltransferase (UGCG).

141 uent C5aR1 activation controlled UDP-glucose ceramide glucosyltransferase production, thereby tipping

142 ids, metabolites, and complex lipids such as ceramides, glycerophosphoglycerols, cardiolipins, and gl

143 e (GCS) is a rate-limiting enzyme catalyzing ceramide glycosylation, thereby regulating cellular cera

144 The bioactive sphingolipid ceramide has emerged as an antitumorigenic lipid, and tr

145 in spin mutants allowed us to conclude that ceramide homeostasis is the driving force in disease pro

146 Mass spectrometry revealed elevations of ceramides, hydroxy-ceramides, dihydroceramides, sphingos

147 ade glucosylceramide (GlcCer) to glucose and ceramide in different cellular compartments.

148 sphingomyelinase and concomitant release of ceramide in endothelial cells treated with the toxin.

149 Instead we propose that the presence of ceramide in one of the membrane monolayers causes a surf

150 To examine the role of ceramide in ovarian cancer metastasis, ceramide liposome

151 n polyunsaturated fatty acids, but decreases ceramide in the cells.

152 endent ceramide synthesis and maintenance of ceramide in the cellular membrane are essential for lame

153 tter) and contained low amounts of bioactive ceramides in a ratio to sphingomyelin of 1:5mol% in butt

154 1 and 2 reduce plasma ceramides in rodents, have a slight trend toward enhance

155 s to study the subcellular redistribution of ceramides in the course of T cell activation.

156 CerS2, a nonneuronal CerS producing C22-C24 ceramides, in neurons of Cers1-deficient mice.

157 C6 ceramide increases IQGAP1 protein levels by preventing i

158 We report here that C6 ceramide increases serum-stimulated ERK1/2 activation in

159 tate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged

160 To determine whether the mechanism of ceramide-induced membrane leakage is consistent with the

161 2), a membrane protein containing a putative ceramide-interacting domain.

162 iposomes, suggesting specific involvement of ceramide interaction with PI3KC2beta in metastasis suppr

163 e hydrolase that catalyzes the conversion of ceramide into fatty acid and sphingosine.

164 e in sphingolipid metabolism that hydrolyzes ceramide into sphingosine, is highly expressed in the in

165 Ceramide is a pro-apoptotic sphingolipid with unique phy

166 Ceramide is a sphingolipid involved in several cellular

167 Accumulation of apical membrane ceramide is necessary and sufficient to induce the actin

168 imits PI3KC2beta-governed cell motility, and ceramide is proposed to serve as a metastasis-suppressor

169 However, excess ceramide is toxic, causing growth arrest and apoptosis.

170 ls, the fatty acyl chain length variation of ceramides is determined by six (dihydro)ceramide synthas

171 yme in the production of the bioactive lipid ceramide, is involved in the pathogenesis of MS; however

172 Activation of ERK1/2 by ceramide, known to increase lysine acetylation, appears

173 sphingosine-1-phosphate and maintained basal ceramide levels after irradiation.

174 This reaction lowers intracellular ceramide levels and concomitantly generates sphingosine

175 e glycosylation, thereby regulating cellular ceramide levels and the synthesis of glycosphingolipids

176 tations in KDSR were associated with reduced ceramide levels in skin and impaired platelet function.

177 unravel the mechanism by which SMSr controls ceramide levels in the ER.

178 ows SMase activity, which leads to increased ceramide levels that can produce pro-inflammatory effect

179 In skeletal muscle, liver, and spleen, C16:0-ceramide levels were altered independent of feeding cond

180 eased expression of FEN1 and SUR4, increased ceramide levels, decreased expression of nutrient transp

181 AC inhibition increased cellular ceramide levels, decreased sphingosine 1-phosphate level

182 Indices of NAFLD, including hepatic ceramide levels, oxidative stress, and expression of pro

183 e fro;5XFAD mice had reduced brain exosomes, ceramide levels, serum anticeramide IgG, glial activatio

184 by genetic or pharmacological correction of ceramide levels-normalizes beta1-integrin distribution a

185 lation of SMPDL3b, and elevation of cellular ceramide levels.

186 icant reduction in long- and very-long-chain ceramide levels.

187 unfolded protein response due to increasing ceramide levels.

188 ibition markedly reduced intestine and serum ceramide levels.

189 he TORC2 network is to modulate synthesis of ceramide lipids, which play roles in signaling.

190 Ceramide liposomes had an inhibitory effect on peritonea

191 le of ceramide in ovarian cancer metastasis, ceramide liposomes were employed and confirmed to suppre

192 down cells was insensitive to treatment with ceramide liposomes, suggesting specific involvement of c

193 all clinical populations have suggested that ceramides may represent an intermediate link between ove

194 aintaining skin barrier function and loss of ceramides may underlie inflammatory and premalignant ski

195 CB2 activation led to ceramide-mediated BC cell apoptosis independently of SL

196 sicular, and their release is independent of ceramide-mediated vesicle secretion.

197 mportance in understanding the regulation of ceramide metabolism in pathogenesis.

198 hanistically, intestine HIF-2alpha regulates ceramide metabolism mainly from the salvage pathway, by

199 pentasaccharide, indicating that neither the ceramide moiety nor the surface of the phospholipid memb

200 Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on

201 observations include unusual localization of ceramides on the endosperm/scutellum boundary and subcel

202 these findings suggest that dysregulation of ceramide pathways and calcium sensitive exocytosis under

203 11.2DS)-related pathways, such as changes in ceramide phosphoethanolamines, sphingomyelin, carnitines

204 e to increased ceramide and the formation of ceramide platforms that trap beta1-integrins on the lumi

205 erm treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an

206 This down-regulation in ceramide production appears to result from suppression o

207 In cancer cells, ASM-mediated ceramide production is important for apoptosis, cell pro

208 CERS6 knockdown in NSCLC cells altered the ceramide profile, resulting in decreased cell migration

209 In vivo ceramide reduction by inhibition of de novo ceramide syn

210 Whether LCB elevation or C18 ceramide reduction leads to neurodegeneration is unclear

211 ogical analysis demonstrated that long-chain ceramide regenerated from C6-ceramide through the salvag

212 The sphingolipid ceramide regulates cellular processes such as differenti

213 crease in LCBs and C16 fatty acid-containing ceramides relative to wild-type plants.

214 lation of LCBs and C16 fatty acid-containing ceramides relative to wild-type plants.

215 Because ceramide release and redistribution occur very rapidly i

216 tudies addressing rapid stimulation-mediated ceramide release in living cells.

217 ause the membrane permeabilizing activity of ceramide remains poorly understood.

218 CS-released EMPs and cMPs were ceramide-rich and required the ceramide-synthesis enzyme

219 Ceramide-rich membrane areas promote structural changes

220 The ordered, palmitoyl ceramide-rich phase started to form above 2 mol % in the

221 0 % of all membrane ceramides are located in ceramide-rich platforms (CRPs) with a size of about 75 n

222 Participants with a higher ceramide score and assigned to either of the 2 active in

223 de score, whereas participants with a higher ceramide score and assigned to the control arm presented

224 The association between baseline ceramide score and incident CVD varied significantly by

225 The ceramide score, calculated as a weighted sum of concentr

226 howed similar CVD risk to those with a lower ceramide score, whereas participants with a higher ceram

227 ndoplasmic reticulum (ER) resident candidate ceramide sensor protein, SMSr/SAMD8.

228 In particular, ceramide serves as an essential building hub for complex

229 h have significantly decreased levels of C16-ceramide, showed that CerS6-deficiency protected against

230 effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif

231 TORC2-dependent control of ceramide signaling strongly influences both cell size an

232 rogen bonding is important for sterol/SM and ceramide/SM interactions, as well as for the lateral seg

233 , and C24:1 ceramides were the most abundant ceramide species detected.

234 r a single dose of radiation (8 Gy), several ceramide species were significantly elevated.

235 ence points toward an important role for the ceramide/sphingosine-1-phosphate rheostat in maintaining

236 l ceramide biosynthesis via deacetylation of ceramide synthase (CerS) 1, 2, and 6.

237 n of ceramides is determined by six (dihydro)ceramide synthase (CerS) isoforms.

238 The subtype ceramide synthase (CerS)6 was specifically up-regulated

239 ACBP increases the activity of ceramide synthase 2 (CerS2) by more than 2-fold and CerS

240 ased levels of maternal transcripts encoding ceramide synthase 2b (Cers2b), and loss of Cers2b in sph

241 specimens and cell lines and determined that ceramide synthase 6 (CERS6) is markedly overexpressed co

242 Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid b

243 A novel role for ceramide synthase 6 in mouse and human alcoholic steatos

244 fferentially regulates functionally distinct ceramide synthase activities as part of a broader sphing

245 es, in contrast, displayed increased class I ceramide synthase activity but reduced class II ceramide

246 amide synthase activity but reduced class II ceramide synthase activity.

247 In cells, pharmacologic inhibition of ceramide synthase reduced lipid accumulation by reducing

248 ound to have reduced activity of the class I ceramide synthase that uses C16 fatty acid acyl-coenzyme

249 fam57ba, encoding a ceramide synthase, was identified as interacting with th

250 phingosine kinase-2, neutral ceramidase, and ceramide synthase-5.

251 Ceramides are synthesized by a family of six ceramide synthases (CerS) in mammals, which produce cera

252 sphingolipid metabolism, is generated by six ceramide synthases (CerS) that differ in substrate speci

253 IR triggers SIRT3-dependent deacetylation of ceramide synthases and the elevation of ceramide, which

254 ll mice, and SIRT3 directly deacetylates the ceramide synthases in a NAD(+)-dependent manner that inc

255 showed that SIRT3-mediated deacetylation of ceramide synthases increased enzyme activity and ceramid

256 ubstrates but increased activity of class II ceramide synthases that use very-long-chain fatty acyl-c

257 these results indicate that CERS6-dependent ceramide synthesis and maintenance of ceramide in the ce

258 l mode of regulation of very-long acyl chain ceramide synthesis by ACBP, which we anticipate is of cr

259 Finally, inhibiting de novo ceramide synthesis improves the response of palmitic aci

260 atment with 1 mm palmitate increases de novo ceramide synthesis in both cell lines to a similar degre

261 We examined the effects of pharmacologic ceramide synthesis inhibition on hepatic PLIN2 expressio

262 gosine reductase), encoding an enzyme in the ceramide synthesis pathway, lead to a previously undescr

263 ceramide reduction by inhibition of de novo ceramide synthesis reduced PLIN2 and hepatic steatosis i

264 ncluding pathways related to redox response, ceramide synthesis, JA, ethylene (ET), salicylic acid (S

265 P) potently facilitates very-long acyl chain ceramide synthesis.

266 chain fatty acids (C24 to C26) required for ceramide synthesis.

267 and cMPs were ceramide-rich and required the ceramide-synthesis enzyme acid sphingomyelinase (aSMase)

268 The specific role of ceramide synthetic enzymes in the regulation of PLIN2 an

269 a novel regulator of PLIN2 and suggest that ceramide synthetic enzymes may promote the earliest stag

270 important role of the acid sphingomyelinase/ceramide system for the endothelial response to toxins a

271 to activate the acid sphingomyelinase (Asm)/ceramide system.

272 ls, melanoma cells generate lower amounts of ceramides than normal melanocytes do.

273 greater accumulation of long-chain saturated ceramides that are substrate for AC.

274 In the presence of ceramide, the N terminus of the first transmembrane doma

275 hich cells prevent the toxic accumulation of ceramides; they facilitate nonvesicular ceramide transfe

276 A treatment of HSCs promoted accumulation of ceramide through inhibition of acid ceramidase (aCDase).

277 that long-chain ceramide regenerated from C6-ceramide through the salvage/recycling pathway, at least

278 se activity that catalyses the hydrolysis of ceramide to produce sphingosine and a free fatty acid (F

279 ncrease both PtdIns(4)P-binding affinity and ceramide transfer activity of a CERT-serine-rich phospho

280 domain decreases both PtdIns(4)P binding and ceramide transfer by CERT.

281 n of ceramides; they facilitate nonvesicular ceramide transfer from the endoplasmic reticulum (ER) to

282 ponse to stress and reveal that nonvesicular ceramide transfer out of the ER prevents the buildup of

283 interface and PI-4P-dependent recruitment of ceramide transfer protein (CERT) for sphingomyelin synth

284 ulum to the Golgi by the multidomain protein ceramide transfer protein (CERT).

285 ed lipid transfer domain (START) carries out ceramide transfer.

286 Ceramide treatment also suppressed cell motility promote

287 Consistent with an increase in ceramide, VPA decreased the expression of amino acid tra

288 timulation of iNKT cells by alpha-galactosyl-ceramide was effective in both preventing and treating c

289 oparticle-based delivery, fluorescent NBD C6-ceramide was efficiently converted to NBD C6-glucosylcer

290 Mechanistically, ceramide was revealed to interact with the PIK-catalytic

291 as a weighted sum of concentrations of four ceramides, was associated with a 2.18-fold higher risk o

292 entrations of C16:0, C22:0, C24:0, and C24:1 ceramides were 2.39 (1.49-3.83, Ptrend<0.001), 1.91 (1.2

293 Azido-functionalized C6-ceramides were incorporated into and localized within pl

294 Ceramides were labeled by immunocytochemistry to visuali

295 In particular, C16:00, C24:00, and C24:1 ceramides were the most abundant ceramide species detect

296 n of ceramide synthases and the elevation of ceramide, which could inhibit complex III, leading to in

297 Ceramide, which serves a central role in sphingolipid me

298 Acid ceramidase (AC) hydrolyzes ceramides, which are central lipid messengers for metabo

299 aft model delayed tumor growth and increased ceramide while decreasing proliferation.

300 e synthases (CerS) in mammals, which produce ceramides with differentN-linked acyl chains.