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1  to sphingosine forming N-acetylsphingosine (C2-ceramide).
2 o sphingosine producing N-acetylsphingosine (C2-ceramide).
3 istant to toxicity from 10 to 100 micromol/L C2 ceramide.
4 ocytes, which subsequently was eliminated by C2-ceramide.
5  JNK activation in MS1418 cells than that by C2-ceramide.
6 hesis and super sensitive to sphingosine and C2-ceramide.
7 ions by generating a variant lipid mediator, C2-ceramide.
8 2, C, or D, mimicked the enhancing effect of C2-ceramide.
9 -10 to inhibit the induction of TNF-alpha by C2-ceramide.
10 ere inhibited by C2-ceramide but not dihydro-C2-ceramide.
11 ated by lung perfusion with exogenous ASM or C2-ceramide.
12 sorbitol, anti-Fas antibody, or TNFalpha and C2-ceramide.
13 rradiation or exposure to the cell permeable C2-ceramide.
14 riate control for the nonspecific effects of C2-ceramide.
15                                              C2-Ceramide (15 microM) inhibited ADP-induced aggregatio
16         By contrast, treatment of cells with C2-ceramide (a potent PP2A activator) or expression of t
17                         N-Acetylsphingosine (C2-ceramide), a cell-permeable short-chain analogue, and
18 curs in the presence of N-acetylsphingosine (C2-ceramide), a synthetic cell-permeable ceramide analog
19 hosphorylation of mu- and m-calpains whereas C2-ceramide, a potent PP2A activator, reduces nicotine-i
20                                We found that C2-ceramide activated JNK and induced growth arrest in m
21                            Although SMase or C2-ceramide alone was ineffective in activating NF-kappa
22                                              C2-ceramide also induced the apoptosis of an AHR-contain
23                                              C2-ceramide also inhibited phosphorylation and activatio
24                                    Moreover, C2-ceramide also inhibited stimulation of Akt by platele
25  Synthetic cell-permeable ceramides (C6- and C2-ceramide) also concentration dependently inhibited DN
26 eated a variety of cell lines with 20 microM C2-ceramide and examined apolipoprotein-mediated cholest
27                     We found that while both C2-ceramide and LPS activated c-Jun N-terminal kinase (J
28 d, SV40-transformed cells cleared 45% of [3H]C2-ceramide and produced C2-SM, which accounted for 24%
29 howed that they blocked apoptosis induced by C2-ceramide and sorbitol, but were not able to block apo
30         Northern blot analyses revealed that C2-ceramide and sphingomyelinase increased interleukin-1
31                                              C2-ceramide and sphingomyelinase induced NF-kappaB activ
32                     Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM
33 n cells were treated with the combination of C2-ceramide and TNF-alpha or IL-1beta.
34 dy, we demonstrate that N-acetylsphingosine (C2-ceramide) and a variety of sphingoid bases (e.g., D-e
35 effects of a cell-permeable ceramide analog (C2-ceramide) and LPS on murine macrophage cell lines and
36 racellular stores (such as arachidonic acid, C2-ceramide, and oxidative stress).
37 of apoptosis by anti-Fas antibody, TNFalpha, C2-ceramide, and thermal shock.
38  transacetylase, and physiological levels of C2-ceramide are detected in both undifferentiated and di
39 6-keto-PGF1 alpha formation was inhibited by C2-ceramide as well as by ethanol treatment.
40                                              C2-ceramide at 5 micron enhanced interleukin-1 beta (IL-
41                                              C2-Ceramide at a ceramide: lipid ratio of 0.2 caused pla
42 pid ratio of 10 was equal to that induced by C2-ceramide at a ratio of 0.2 (approximately 3%).
43                Platelet lysis was induced by C2-ceramide at higher ceramide:lipid ratios (0.5), where
44                                              C2-ceramide, at concentrations which antagonized activat
45              An inhibitor of PLD activation, C2-ceramide, attenuated ET-1-induced PLD activity, as in
46           The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indi
47 tivation and degranulation were inhibited by C2-ceramide but not dihydro-C2-ceramide.
48                        Results indicate that C2-ceramide but not inactive C2-dihydroceramide, was fou
49 cation of a cell permeable ceramide analogue C2 ceramide, but not the biologically inactive C2 dihydr
50 c7 cells also arrested following exposure to C2-ceramide, but did not undergo apoptosis.
51 area/anterior hypothalamic neurons show that C2-ceramide, but not dihydroceramide, mimics the rapid h
52 events apoptosis induced by camptothecin and C2-ceramide by phosphorylating BAD on Ser-112 in a prote
53                                              C2-Ceramide caused nearly total leakage of dye from the
54 re of 1c1c7 cultures to N-acetylsphingosine (C2-ceramide) caused a concentration-dependent inhibition
55          We report here that (1) exposure to C2-ceramide (cer) rarely increases OLG Cai, whereas sphi
56 rthermore, the inhibition of phagocytosis by C2-ceramide correlated with the inhibition of tyrosine p
57 alkaline hydrolysis, and ability to form the C2-ceramide dibenzoate derivative.
58                                              C2-ceramide did not inhibit insulin-stimulated phosphory
59 meabilized PMNs stimulated with GTP gamma S, C2-ceramide did not inhibit RhoA translocation.
60                          Treating cells with C2-ceramide does not affect phosphorylation of insulin r
61 LPS-induced cell death and less sensitive to C2 ceramide-evoked cytotoxicity, when compared with Lps(
62                   Unlike lipopolysaccharide, C2-ceramide failed to activate NF-kappaB and did not ind
63 ch as diacylglycerol, phosphatidic acid, and C2-ceramide, failed to induce a significant increase in
64     Pretreatment of C3H/OuJ macrophages with C2-ceramide greatly diminished AP-1 induction following
65 ontrast, N-acetyldihydrosphingosine (dihydro-C2-ceramide) had no effect on either tyrosine phosphoryl
66                        Collectively, because C2-ceramide has many biological activities that differ f
67 eed in the absence of p53, exogenously added C2-ceramide increased the cellular p53 level in LM cells
68                                              C2-Ceramide induced a larger decrease in anisotropy than
69 cells, Fas ligation or addition of exogenous C2-ceramide induced activations of caspase-3/CPP32 and c
70  and its downstream substrates, and inhibits C2-ceramide induced apoptosis.
71                     Synthetic cell permeable C2-ceramide induced apoptotic death of rat neonatal card
72 ted of c-Fos, Jun-B, Jun-D, and c-Jun, while C2-ceramide induced Jun-D and c-Jun only.
73 PS and the cell-permeable ceramide analogue, C2 ceramide, induced significant cell death in IFN-gamma
74 tion of NF-kappaB and AP-1 but did not block C2-ceramide-induced AP-1.
75 ip between AHR content and susceptibility to C2-ceramide-induced apoptosis.
76 t constitutively active Akt kinase decreases C2-ceramide-induced death of HMN1 cells as well as COS-7
77                                 Importantly, C2-ceramide-induced suppression of calpain phosphorylati
78                                  Strikingly, C2 ceramide induces, whereas its phosphorylated derivati
79                           Our data show that C2-ceramide induces apoptosis in HMN1 motor neuron cells
80  of studies, the short-chain ceramide analog C2-ceramide inhibited insulin-stimulated glucose transpo
81      Prior incubation of PMNs with 10 microM C2-ceramide inhibited PLD activity and RhoA translocatio
82                         N-Acetylsphingosine (C2-ceramide) inhibited phagocytosis, reduced ERK1 and ER
83  fluidity of lipid vesicles all suggest that C2-ceramide inhibits platelet aggregation because it des
84 ramide did not induce lysis, suggesting that C2-ceramide is able to destabilize membranes.
85                                              C2-ceramide is produced via PAF:sphingosine transacetyla
86                      Here, membrane permeant C2-ceramide is shown to attenuate the basal and insulin-
87 treated with D-erythro-MAPP prior to feeding C2 ceramide manifest markedly elevated levels of apoptos
88                                    Exogenous C2-ceramide markedly increased apoptosis in quiescent Ve
89 tment inhibited both lipopolysaccharide- and C2-ceramide-mediated responses.
90 thalamic application of the cell-penetrating C2-ceramide mimics the rapid phase of the IL-1beta-induc
91                          The ceramide analog C2-ceramide (N-acetylsphingosine) was without effect on
92            This indicates that the effect of C2-ceramide on ADP-induced platelet aggregation depends
93 ase activity, suggesting that the effects of C2-ceramide on Akt kinase are not mediated through modul
94 of iNOS, we examined the effect of SMase and C2-ceramide on the activation of NF-kappaB.
95                        Addition of exogenous C2 ceramide or bacterial-derived sphingomyelinase to alv
96         Moreover, we report that addition of C2-ceramide or D-erythrosphingosine to neutrophils after
97                               Treatment with C2-ceramide or sphingomyelinase did not alter NF-ELAM1 s
98       Lipopolysaccharide and, less potently, C2-ceramide or sphingomyelinase, stimulated AP-1-depende
99 resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide).
100 is factor alpha (TNFalpha), antibody to Fas, C2-ceramide, osmotic shock (sorbitol), and thermal shock
101                                              C2 ceramide plus IFN-gamma failed to activate release of
102 ed the nonspecific effects on membranes that C2-ceramide possessed, suggesting that C2-dihydroceramid
103 dominant-negative FAN--expressing cells with C2-ceramide produced substantial cell death, indicating
104 ml(-1) NGF or 1 microM N-acetyl sphingosine (C2-ceramide) produced a 3- to 4-fold increase in the num
105 ine-phospholipase D (PC-PLD), butan-1-ol and C2 ceramide, produced marked inhibition of constitutive
106 atment, normal WI38 cells cleared 17% of [3H]C2-ceramide producing [3H]C2-SM, which accounted for 13%
107 ort that apoptotic stimuli (staurosporine or C2-ceramide) reciprocally altered Bcl-x splicing in neur
108      Moreover, non-toxic levels of exogenous C2-ceramide sensitized LNCaP cells to irradiation simila
109 C), etoposide, or sphingoid bases (including C2 ceramide, sphingosine, or sphinganine) caused the acc
110 xogenously-added sphingolipids (sphingosine, C2-ceramide, sphingosine 1-phosphate, and N,N-dimethylsp
111 hed by its identical Rf value with authentic C2-ceramide standard on thin-layer plate, sensitivity to
112 minished AP-1 induction following subsequent C2-ceramide stimulation.
113  by IL-1 beta differs from that activated by C2-ceramide, suggesting that signaling pathways utilized
114     However, apoptosis could be induced with C2-ceramide, suggesting that signals proximal to the gen
115                               The ability of C2-ceramide to cause platelet fenestrations, formation o
116                          The addition of [3H]C2-ceramide to cells resulted in a time-dependent format
117 or modulated the development of apoptosis in C2-ceramide-treated 1c1c7 cultures.
118 dissociate Bax from isolated mitochondria of C2-ceramide-treated cells.
119 ia were measured with fluorescent markers in C2-ceramide-treated primary cultures of mesencephalic ne
120 modes including tumor necrosis factor alpha, C2-ceramide, UV irradiation, and serum deprivation.
121 osis induced by tumor necrosis factor alpha, C2-ceramide, UV irradiation, or serum deprivation.
122                                              C2-ceramide was also unable to activate NF-kappaB, a tra
123                       Furthermore, exogenous C2-ceramide was cytotoxic to bovine brain endothelial ce
124 des with short fatty acyl groups-d18:1-C2:0 (C2-ceramide, where d18:1 is sphingosine and C2:O is an a
125 8 cells by exposure of the cells to SMase or C2-ceramide, whereas phospholipase A2 or phospholipase C
126       Conversely, overexpression of Smpd3 or C2-ceramide, which mimics the function of nSMase2, inhib
127  respiratory chain complex III is reduced by C2-ceramide with half-maximum effect at 5-7 microM.
128                                              C2-Ceramide without FFA induced DNA laddering, but fumon

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