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1 es on longevity (leukemia inhibitory factor, ceramides).
2 ansport reduced the efflux of exogenous C(6)-ceramide.
3 gomyelinase that hydrolyzes sphingomyelin to ceramide.
4 ydrolysis of glucosylceramide to glucose and ceramide.
5 DHA) and accumulated more lipid droplets and ceramide.
6  emphysema is associated with increased lung ceramide.
7 glycolipid glucosylceramide into glucose and ceramide.
8 n attached to a hydrophobic membrane anchor, ceramide.
9  the availability of nutrients and lysosomal ceramide.
10 odulated by competition with nonglycosylated ceramides.
11 he accumulation of IR-related carnitines and ceramides.
12 eloped to comprehensively quantify zebrafish ceramides.
13 ggrin and filaggrin-2, as well as long-chain ceramides.
14 lts in increases in cellular sphingosine and ceramides.
15 ups of diacylglycerols, triacylglycerols and ceramides.
16 es de novo SL production and increases liver ceramides.
17 glycerides, diglycerides, sphingomyelins and ceramides.
18 s was accompanied by accumulation of cardiac ceramides.
19                             The sphingolipid ceramide 1-phosphate (C1P) directly binds to and activat
20  active sphingolipids resulting in decreased ceramide-1-phosphate (C1P) content as observed in human
21                       In contrast, levels of ceramide-1-phosphate (C1P) dropped in a time-dependent m
22 sphoinositides, diacylglycerolpyrophosphate, ceramide-1-phosphate, and phosphatidic acid belong to a
23 sphingolipids, including phosphatidylserine, ceramide-1-phosphate, glucosylceramide, and sulfatide, v
24 ssociated with HF risk in both cohorts: CER (ceramide) 16:0 (relative risk [RR] per SD in PREDIMED, 1
25 es (PCs), 7 lysophosphatidylethanolamines, 5 ceramides, 3 branched chain amino acids, and 9 neurotran
26                                              Ceramides, a type of sphingolipid (SL), have been implic
27                                              Ceramide accumulation determined by liquid chromatograph
28 ighlights the article by Li et al that links ceramide accumulation in podocytes to cellular damage an
29 ed reduced size, early mortality, and severe ceramide accumulation where the amplitude of ceramide ch
30 xpression, which stimulates NOX4 expression, ceramide accumulation, and causes DbCM.
31 n alleviated superoxide formation, prevented ceramide accumulation, and improved cardiac function in
32                 Mechanistic studies revealed ceramide actions that promoted lipid uptake and storage
33                  Mechanistically, PP2A-Cdc55 ceramide-activated phosphatase was found to act downstre
34 tion, the results revealed that this pool of ceramide acutely regulates cell adhesion and cell migrat
35             Acyl chain length alterations in ceramides also suggested roles for FATP4 in esterifying
36 ge of sphingomyelin to phosphorylcholine and ceramide, an essential step in the formation and release
37                     UGCG inhibition with the ceramide analog d-threo-1-(3,4,-ethylenedioxy)phenyl-2-p
38 F-HPA-12, a radio-fluorinated version of the ceramide analog N-(3-hydroxy-1-hydroxymethyl-3-phenylpro
39 -PLs) and palmitoyl ceramide (PCer) or other ceramide analogs in dioleoylphosphatidylcholine (DOPC) b
40                                              Ceramide analogs like HPA-12 may function as metabolic p
41 fter screening a series of newly synthesized ceramide analogs, here, we have identified compounds wit
42           Processes that can be regulated by ceramide and are important for severity of allergic asth
43 fication of specific and different roles for ceramide and ASM secreted by irradiated endothelial cell
44 ase 2 (nSMase2) produces the bioactive lipid ceramide and has important roles in neurodegeneration, c
45                          Here we report that ceramide and its related enzyme acid sphingomyelinase (A
46 an excessive, more than 130-fold increase in ceramide and other sphingolipids.
47  counteract the negative effects of elevated ceramide and promote cell survival, thereby providing ca
48 osphatidylcholine, phosphatidylethanolamine, ceramide and sphingomyelin lipid groups, for example, in
49 in Alzheimer's disease (AD) brain leading to ceramide and sphingosine accumulation and reduced levels
50 responsive to the pro-apoptotic sphingolipid ceramide and that this response is strictly stereospecif
51                                              Ceramide and the two isoforms of ASM were acutely secret
52 umption with concentrations of 3 circulating ceramides and ceramide ratios.
53                The meC18SO is metabolized to ceramides and complex SLs and is a constituent of human
54 ted accumulation of lipotoxic intermediates (ceramides and diacylglycerols) and reduced reactive oxyg
55 d elevations in myocardial free fatty acids, ceramides and diacylglycerols, consistent with developme
56 loped marked elevations in free fatty acids, ceramides and diacylglycerols.
57                             Several of these-ceramides and glucosylceramides-induced differentiation
58  key enzymes that regulate the metabolism of ceramides and glycosphingolipids, which are important me
59 vonic acid enrichment led to increased C24:1-ceramides and improved several metabolic parameters incl
60 esis of cardiotoxic C16- and C24-, and C24:1 ceramides and increased potentially cardioprotective C20
61                         It is concluded that ceramides and lyso-PLs associated with each other both i
62            Lower levels of sphingolipids and ceramides and other metabolomic alterations observed in
63 a conserved double bond into the backbone of ceramides and other predominant sphingolipids.
64 tissues revealed an abnormal accumulation of ceramides and other sphingolipids.
65              Prominent sphingolipids include ceramides and sphingosine-1-phosphate that regulate mult
66 centrations that depend on the nature of the ceramides and the co-phospholipids.
67 w opportunities to probe the causal roles of ceramides and their metabolic derivatives in a wide arra
68 , molecular details of the SET-FTY720 or SET-ceramide, and mechanism of FTY720-dependent PP2A activat
69 aluated immune response, Oil Red-O staining, ceramide, and triacylglycerol levels.
70  phospholipids, neutral lipids, cholesterol, ceramides, and free fatty acids.
71  beyond the seedling stage, hyperaccumulated ceramides, and showed altered organellar structures and
72 allergic asthma had higher dihydroceramides, ceramides, and sphingomyelins compared with children wit
73 nallergic asthma had lower dihydroceramides, ceramides, and sphingomyelins than did controls.
74                            Free fatty acids, ceramides, and triacylglycerol classes in plasma correla
75                                              Ceramides are central intermediates of sphingolipid meta
76 types that accumulate, sphingolipids such as ceramides are particularly impactful, as they elicit the
77 inantly acylated to sphingolipids, including ceramides, are selectively reduced in a mouse model of o
78 ve therapy for CLN3 disease and use of serum ceramide as a potential biomarker to track impact of the
79 ions, and the results define plasma membrane ceramide as an acute signaling effector necessary and su
80       This study identifies secreted ASM and ceramide as paracrine factors enhancing intestinal epith
81  scores.CONCLUSIONThis study validates serum ceramides as candidate biomarkers of CVD and suggests th
82 e (ASMase) and generate the second messenger ceramide at plasma membranes, triggering apoptosis in sp
83 ramide upon chemotherapy treatment, and both ceramide at the plasma membrane and nSMase2 were necessa
84 ant enzymes to mimic physiological levels of ceramide at the plasma membrane upon chemotherapy treatm
85 tivate iNKT cells is highly dependent on the ceramide backbone structure.
86 nthetic GM3 and GD3 comprising a d18:1-C24:1 ceramide backbone were able to activate iNKT cells in a
87  ceramide species that are included in other ceramide-based scores.CONCLUSIONThis study validates ser
88 at Asp(147) or Asn(169) of RIPK1 are key for ceramide binding and that Arg(258) or Leu(293) residues
89 on channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins.
90                                       FTY720-ceramide binding resulted in chemical shifts of residues
91 mulations reveal that both channels harbor a ceramide binding site on one side of the barrel wall.
92 likely serve as measures of flux through the ceramide biosynthesis pathway rather than the abundant d
93 e (GlcCer), the initial GSL synthesized from ceramide by GCS (GlcCer synthase), is required for embry
94 ceramide synthesis were upregulated and that ceramide (C16, C20, C20:1, and C24) levels had significa
95 pendent variable) to blood concentrations of ceramides (C16:0, C22:0, and C24:0) and ceramide ratios
96 e report on clickable, azobenzene-containing ceramides, caCers, as photoswitchable metabolic substrat
97 re are reports that Chol is able to displace ceramide (Cer) in SM bilayers and abolish the S(o) phase
98 melting of the interior slab, which contains ceramide (Cer) in the posturing chain conformation, a st
99 we quantified sphingolipids including SM and Ceramide (Cer) using Multiple Reaction Monitoring (MRM),
100 d by the saturated fatty acid carried by the ceramide (Cer).
101                                              Ceramides (Cer) and cerebrosides are important sphingoli
102 win model (h(2) = 0.28-0.59), which included ceramides (Cer) and triglycerides (TG).
103 ceramide accumulation where the amplitude of ceramide change depended on both acyl chain and LCB leng
104 esis identified developmental stage-specific ceramide changes based on long chain base (LCB) length.
105 holipids and increasing long-chain saturated ceramides, changes previously linked to apoptosis.
106 d decreased proportions of these and the two ceramide classes that carry ultralong-chain, amide-linke
107 lize UGCG and have increased GSL content for ceramide clearance, which ultimately contributes to chem
108 lusion, our findings indicate that the RIPK1-ceramide complex forms large membrane pores we named cer
109 eceptor-interacting Ser/Thr kinase 1 (RIPK1)-ceramide complex transported to the plasma membrane by n
110 olution examination of the SET-FTY720 or SET-ceramide complexes by NMR spectroscopy.
111 cell line demonstrated remarkable overlap in ceramide composition, but also revealed a surprising lac
112 ycerols, and diacylglycerols, although lower ceramide concentrations, in subcutaneous tissue.
113 c lipid metabolism may influence circulating ceramide concentrations.
114 y fatty acids and sphingosines (Cer[NS]) and ceramides containing a-hydroxy fatty acids and sphingosi
115                 In the SC ceramide profiles, ceramides containing nonhydroxy fatty acids and 6-hydrox
116 cids and 6-hydroxysphingosines (Cer[NH]) and ceramides containing nonhydroxy fatty acids and phytosph
117 ytosphingosines (Cer[NP]) increased, whereas ceramides containing nonhydroxy fatty acids and sphingos
118  of Ahr knockout mice exhibited both reduced ceramide content and reduced myelin thickness.
119                                              Ceramides contribute to the lipotoxicity that underlies
120                      'Benzoate metabolism', 'ceramides', 'creatine metabolism', 'fatty acid metabolis
121                In particular, the long-chain ceramides d18:1/20:0 and d18:1/24:0 were elevated and li
122 sociation between a genetically instrumented ceramide (d18:1/20:1) and T2D (odds ratio: 1.15 [95% CI
123 n novel and 3 reported sphingolipids, namely ceramides (d18:1/18:1, d18:1/20:0, d18:1/20:1, d18:1/22:
124 o the pathogenesis of atopic dermatitis as a ceramide-deficient disease.
125  cancer cell catabolism of sphingomyelins to ceramide derivatives and 3) altered ceramide metabolism
126 ain groups detected were phenolic compounds, ceramides, diacylglycerols and triacylglycerols.
127 12 may function as metabolic probes to study ceramide disbalance in the brain.
128                                              Ceramides draw wide attention as tumor suppressor lipids
129                                              Ceramide elevation drives local bilayer reorganization i
130                      Adding exogenous ASM or ceramide enhanced epithelial cell growth arrest and deat
131 nalog drug FTY720, we show that formation of ceramide-enriched membrane pores, referred to here as ce
132  roles in stress-mediated necroptosis, these ceramide-enriched pores also regulate membrane integrity
133 erified omega-hydroxy fatty acid sphingosine ceramides (EOS-CERs) to nonhydroxy fatty acid sphingosin
134                Progress in understanding how ceramides execute their biological roles is hampered by
135 ath, providing a molecular framework for how ceramides exert their anti-neoplastic activity.
136                                              Ceramides exhibit multiple biological activities that ma
137                    Epidermal lipids, such as ceramides, fatty acids (FAs), triglycerides, and cholest
138 tical role in ZIKV replication and show that ceramide flux is a key mediator of ZIKV infection.
139                   Sphingomyelinases generate ceramide from sphingomyelin as a second messenger in int
140 ith weak connections to commonly established ceramide functions (eg, cell death).
141            The matrix lipids, especially the ceramide-generated sphingosine 1-phosphate, are the mess
142  only enzyme known to hydrolyze proapoptotic ceramide, generates sphingosine, which is then phosphory
143 upregulation of Smpd3, which encodes for the ceramide-generating enzyme neutral sphingomyelinase 2.
144 ic NLPs bind to glycosyl inositol phosphoryl ceramide (GIPC) sphingolipids that are abundant in the o
145 regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.
146 the analysis of GSL-derived glycans based on ceramide glycanase digestion, 8-aminopyrene-1,3,6-trisul
147                                              Ceramides have been implicated in the pathogenesis of ty
148 tamate that mediates direct contact with the ceramide head group.
149 idase (Ac) has been shown to be critical for ceramide hydrolysis and regulation of lysosome function
150  crucial role in the metabolism of lysosomal ceramides, important members of the sphingolipid family,
151 ed by performing behavioral tests, measuring ceramide in brains and serum, and assessing impact on lo
152 sought to investigate the functional role of ceramide in mouse models of allergic airway disease that
153 y, lipidomics analyses showed that increased ceramides in PKM2-activated T-cell EVs were mainly respo
154                       Thus, PKM2-mediated EV ceramides in T cells may be an important cargo for T-cel
155 prising lack of most sphingadiene-containing ceramides in the zebrafish.
156 we measured sphingolipids (including S1P and ceramides) in AML and control cells.
157 est vital roles of sphingolipids, especially ceramides, in the pathogenesis of type 2 diabetes (T2D)
158 ts for each gene, accumulated high levels of ceramide, indicative of unregulated sphingolipid biosynt
159 ent of neurons with medium supplemented with ceramides, induced a time-dependent increase of the tran
160 uman colon cancer cells largely resistant to ceramide-induced apoptosis.
161                                              Ceramide-induced endothelial cell apoptosis boosts intes
162                 Notably, the drug rescued C2 ceramide-induced ER stress-mediated apoptosis and ER str
163                                  Remarkably, ceramide-induced RIP of cAMP response element-binding pr
164   In MVBs, acid ceramidase (aCDase) converts ceramide into sphingosine and increases the formation of
165              Acid ceramidase (AC) hydrolyzes ceramides into sphingoid bases and fatty acids.
166                                              Ceramide inverts the orientation of newly synthesized TM
167 hingomyelinase (SMPD1) and the generation of ceramide is a critical regulator of apoptosis in respons
168 murine models.Measurements and Main Results: Ceramide is increased in cystic fibrosis airway epitheli
169    This is the first time a specific pool of ceramide is interrogated for acute signaling functions,
170                            The metabolism of ceramides is deregulated in the brain of Alzheimer's dis
171 t manner although mRNA and protein levels of ceramide kinase (CERK) remained stable.
172 nal ceramide metabolism, specifically in the ceramide kinase like (CERKL) gene.
173 ingolipid analog drug fingolimod (FTY720) or ceramide leads to the reactivation of tumor suppressor P
174           Our data suggest that elevation of ceramide level after allergen challenge contributes to t
175 t had no significant effects on elevation of ceramide level or apoptosis, indicating that the increas
176 IP re-expression in leukemia cells increased ceramide levels 2-fold, inactivated the key signaling pr
177                              Brain and serum ceramide levels as well as apoptosis rates were lower in
178 es to ZIKV replication sites, and increasing ceramide levels by multiple pathways sensitizes cells to
179 tosis, indicating that the increases in lung ceramide levels in allergen-challenged mice are not medi
180 rogliosis, and diminution in brain and serum ceramide levels in Cln3 (Deltaex7/8) knock-in mice.
181                                The increased ceramide levels in mammalian heart tissues during acute
182                                         Thus ceramide levels in the CSF of patients with progressive
183 nown about the mechanisms by which increased ceramide levels in the lung contribute to allergic respo
184 cell processes like apoptosis, cell membrane ceramide levels increase markedly because of the activat
185 rity of allergic asthma were correlated with ceramide levels measured by mass spectrometry.
186              Prevention of increases in lung ceramide levels mitigated allergen-induced apoptosis, re
187 g attempts to develop therapeutics to reduce ceramide levels to combat metabolic disease.
188 ) mice the allergen-induced increase in lung ceramide levels was significantly reduced, whereas total
189 wn-regulation in AML reduces SK activity and ceramide levels, an effect that ultimately inhibits apop
190 ulation caused SMPD3 upregulation, increased ceramide levels, and inhibited the tumorigenic activity
191                    ORMDL3 regulates systemic ceramide levels, but genetically interfering with Ormdl3
192                                              Ceramide levels, in particular C16 ceramide, were rapidl
193 ost-MI after AC modRNA delivery to decreased ceramide levels, lower cell death rates, and changes in
194                         LCKD decreased C22:1-ceramide levels, which are reported to be high in pancre
195 unoreactivity inversely related to SMPD3 and ceramide levels.
196 almitoyl transferase in response to elevated ceramide levels.
197 o-PC, similarly to PCer, suggesting that the ceramide/lyso-PL interaction was not sensitive to struct
198                                              Ceramides may inhibit the expression of PEMT by increase
199 ham Heart Study's Offspring Cohort who had 3 ceramides measured (n = 1561, mean age 66 y, 59% women).
200 upport a role of VDAC2 as direct effector of ceramide-mediated cell death, providing a molecular fram
201      Use of enteroid models revealed ASM and ceramide-mediated deleterious mode-of-action: when ceram
202        Here, we further examined the role of ceramide-mediated signaling in hepatic dyslipidemia caus
203                             However, how the ceramide metabolism changes over time in AD, in vivo, re
204         Our data gives additional proof that ceramide metabolism is different in FAD mice compared to
205 elins to ceramide derivatives and 3) altered ceramide metabolism that results in increased glycosphin
206       We investigated the effect of altering ceramide metabolism through a loss (chemical inhibitors)
207 herin, its abundance in circulation, role in ceramide metabolism, and homology to C1q suggest an over
208 n patients with mutations that alter retinal ceramide metabolism, specifically in the ceramide kinase
209 rough regulation of ceramide synthesizing or ceramide metabolizing enzymes and dramatically suppress
210                                              Ceramide might be the trigger of formation of Creola bod
211 interactions between the oligosaccharide and ceramide moieties of GT1b and the juxtamembrane and tran
212 t sensitive to structural alterations in the ceramide molecule.
213 lls with a Golgi staining reagent, NBD C(6) -ceramide, NIR imaging in the Golgi apparatus has been de
214 S-CERs) to nonhydroxy fatty acid sphingosine ceramides (NS-CERs) in the skin.
215 bilization in the presence of Chol or oleoyl-ceramide (OCer).
216 ulate sphingomylinases and increase cellular ceramide, often linked to the induction to cell death.
217  associated with concentrations of the C24:0 ceramide only in individuals with prediabetes or diabete
218 without significant changes in inflammation, ceramide or diglyceride contents, endoplasmic reticulum
219                         Here, we report that ceramide or related sphingolipids might invert the topol
220 er total diacylglycerol (P = 0.123) or total ceramides (P = 0.150).
221 bolism and increased intracellular levels of ceramide, paralleled by a nonredundant upregulation of S
222 r lysophospholipids (lyso-PLs) and palmitoyl ceramide (PCer) or other ceramide analogs in dioleoylpho
223  palmitoyl sphingomyelin (PSM) and palmitoyl ceramide (PCer).
224 gesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways.
225                                              Ceramide perturbations may cause adaptive alterations in
226 us to identify an elevation in the levels of ceramide phosphates and sphingosine phosphates in tumor
227 agnostic potential and clinical relevance of ceramide phosphates in breast cancer.
228 tabase comprises sphingomyelin, cerebroside, ceramide, phosphatidylethanolamine, phosphatidylcholine,
229  Bacteroides-derived sphingolipids including ceramide phosphoinositol and deoxy-sphingolipids.
230  consumption and concentrations of the C24:0 ceramide (Pinteraction = 0.014).
231 c dexamethasone treatment induces an ANGPTL4-ceramide-PKCzeta axis that activates hepatic de novo lip
232  in intestinal inflammation and altered host ceramide pools in mice.
233 ed potentially cardioprotective C20- and C22-ceramides post-TAC.
234                     Using a photoactivatable ceramide probe, we here identify the voltage-dependent a
235 shes photolabeling of both channels with the ceramide probe.
236 inase-2 (nSMase2: SMPD3) is a key enzyme for ceramide production involved in inflammation, we investi
237 ptosis, cell-cycle arrest, and intracellular ceramide production through regulation of ceramide synth
238 on and stretch, and its inhibition prevented ceramide production, LC3B-II formation, LC3B/first apopt
239 dings on the regulatory pathways controlling ceramide production, the molecular mechanisms linking th
240 e required for dexamethasone-induced hepatic ceramide production.
241 the penetrated pCer contributes to shift the ceramide profile from an atopic dermatitis to a healthy
242  pathophysiological linkages between altered ceramide profiles in the stratum corneum (SC) of patient
243                                    In the SC ceramide profiles, ceramides containing nonhydroxy fatty
244                          Ventilation-induced ceramides promote autophagy-mediated cell death, and ide
245 d with concentrations of the C16:0 and C22:0 ceramides (Ptrend < 0.05).
246 s of ceramides (C16:0, C22:0, and C24:0) and ceramide ratios (C22:0/C16:0 and C24:0/C16:0).
247 oncentrations of 3 circulating ceramides and ceramide ratios.
248               Additionally, the sphingolipid ceramide redistributes to ZIKV replication sites, and in
249 de-mediated deleterious mode-of-action: when ceramide reduced the number of intestinal crypt-forming
250 combinant human acid ceramidase, to decrease ceramide, reduced both inflammatory mediator production
251                  We previously reported that ceramide regulates a transmembrane protein called TM4SF2
252  is strictly stereospecific, indicating that ceramide regulates the ORMDL-SPT complex via a specific
253 r mean concentrations of the C16:0 and C22:0 ceramides, respectively.
254               In DOPC bilayers, PCer forms a ceramide-rich phase at concentrations above 10 mol%.
255  PCer is known to segregate laterally into a ceramide-rich phase at concentrations that depend on the
256 ion drives local bilayer reorganization into ceramide-rich platforms, macrodomains (0.5-5-um diameter
257 t for socioeconomic and lifestyle factors, a ceramide score (RR Q4 versus Q1 = 2.40; 95% CI: 1.24, 4.
258 re used to demonstrate the role of lysosomal ceramide signaling pathway in AMC.
259 ory lipidomic study that identified specific ceramide species as differentially abundant in the CSF o
260                             SKI-II increased ceramide species but decreased sphingomyelin and sphingo
261 pathway rather than the abundant deleterious ceramide species that are included in other ceramide-bas
262                           Moreover, specific ceramide species were altered in bronchoalveolar lavage
263  dose of radiation, long and very-long-chain ceramide species, and the expression levels of SMPDL3b w
264 ility that higher concentrations of distinct ceramide species, previously associated with adverse met
265 1 and WaGa cells myriocin decreased cellular ceramide, sphingomyelin, and sphingosine-1-phosphate con
266 cant accumulation of sphingolipids including ceramides, sphingosine and sphingosine 1-phosphate (S1P)
267 its glycosphingolipid receptor, GM1, and the ceramide structure of GM1 is likely not a determinant of
268               We show that epidermal loss of ceramide synthase 4 first disturbs epidermal lipid metab
269 onged barrier dysfunction induced by loss of ceramide synthase 4 induced a barrier repair response th
270 rrier and functionally identify differential ceramide synthase 4 protein expression as one key differ
271 ssociated with CGG repeats, such as Schlank (ceramide synthase), Sk2 (sphingosine kinase) and Ras (IM
272 ionally, the impact of galactosylceramide on ceramide synthesis enzymes is documented.
273  DEGS1, which catalyzes the last step in the ceramide synthesis pathway.
274 found that several genes involved in de novo ceramide synthesis were upregulated and that ceramide (C
275 or of the rate-controlling enzyme of de novo ceramide synthesis, serine palmitoyltransferase long-cha
276 bserved with the direct inhibition of SPT or ceramide synthesis.
277 ar ceramide production through regulation of ceramide synthesizing or ceramide metabolizing enzymes a
278 chondrial ROS induce production of lysosomal ceramide that ultimately activates the cytosolic protein
279  of which could be recapitulated by (dihydro)ceramides that lacked the critical double bond.
280 ma by modulating the levels of intracellular ceramide, thus providing novel opportunities for melanom
281 PCer with lyso-PLs was driven by the need of ceramide to obtain a large-headgroup co-lipid, and satur
282 d intracellular and extracellular functions (ceramide trafficker and protein kinase).
283 e to the maintenance of ERTGoCS, such as the ceramide transfer protein CERT and several members of th
284 response to ventilation and stretch, and C16 ceramide treatment of FRLE cells induced autophagy and a
285 nsible for the generation of plasma membrane ceramide upon chemotherapy treatment, and both ceramide
286 pathophysiological linkage by microanalyzing ceramides using normal phase liquid chromatography-elect
287                         Interestingly, serum ceramide was not enhanced in irradiated ASMKO mice, whic
288  possible functions of this specific pool of ceramide, we used recombinant enzymes to mimic physiolog
289 rmore, other bioactive sphingolipids such as ceramide were also down-regulated in primary AML cells.
290 y complexes containing palmitoyl lyso-PC and ceramide were prepared, and these had a bilayer structur
291                                  Because ASM/ceramide were secreted by primary endothelial cells, the
292             Whole-blood dihydroceramides and ceramides were decreased in subjects with the 17q21 asth
293           Ceramide levels, in particular C16 ceramide, were rapidly elevated in response to ventilati
294 um, levels of total sphingolipids, including ceramides, were increased in Ormdl3(-/-) mice, whereas t
295 icin and vorinostat still increased cellular ceramide, which was located predominantly at the plasma
296 essed cells increase de novo biosynthesis of ceramides, which return to sub-toxic levels after UGCG m
297 f phosphatidylethanolamines and glycosylated ceramides, which were poorly detected in MALDI-MSI.
298                 Sphingosine, a metabolite of ceramide with antimicrobial properties, is not upregulat
299 ted significantly lower levels of glomerular ceramide with decreased podocyte injury compared with As
300                   ACSL1 trafficked LCFA into ceramides without normalizing the reduced triglyceride s

 
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