ライフサイエンスコーパス: C2-ceramide

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 JNK activation in MS1418 cells than that by C2-ceramide.

5 ions by generating a variant lipid mediator, C2-ceramide.

6 2, C, or D, mimicked the enhancing effect of C2-ceramide.

7 hesis and super sensitive to sphingosine and C2-ceramide.

8 -10 to inhibit the induction of TNF-alpha by C2-ceramide.

9 ocytes, which subsequently was eliminated 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 1-phosphate (S1P) and partially prevented by C2-ceramide and an agonist of S1P-receptor 1 (S1PR1); th

27 eated a variety of cell lines with 20 microM C2-ceramide and examined apolipoprotein-mediated cholest

28 We found that while both C2-ceramide and LPS activated c-Jun N-terminal kinase (J

29 d, SV40-transformed cells cleared 45% of [3H]C2-ceramide and produced C2-SM, which accounted for 24%

30 howed that they blocked apoptosis induced by C2-ceramide and sorbitol, but were not able to block apo

31 Northern blot analyses revealed that C2-ceramide and sphingomyelinase increased interleukin-1

32 C2-ceramide and sphingomyelinase induced NF-kappaB activ

33 Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM

34 n cells were treated with the combination of C2-ceramide and TNF-alpha or IL-1beta.

35 dy, we demonstrate that N-acetylsphingosine (C2-ceramide) and a variety of sphingoid bases (e.g., D-e

36 effects of a cell-permeable ceramide analog (C2-ceramide) and LPS on murine macrophage cell lines and

37 racellular stores (such as arachidonic acid, C2-ceramide, and oxidative stress).

38 of apoptosis by anti-Fas antibody, TNFalpha, C2-ceramide, and thermal shock.

39 transacetylase, and physiological levels of C2-ceramide are detected in both undifferentiated and di

40 6-keto-PGF1 alpha formation was inhibited by C2-ceramide as well as by ethanol treatment.

41 C2-ceramide at 5 micron enhanced interleukin-1 beta (IL-

42 C2-Ceramide at a ceramide: lipid ratio of 0.2 caused pla

43 pid ratio of 10 was equal to that induced by C2-ceramide at a ratio of 0.2 (approximately 3%).

44 Platelet lysis was induced by C2-ceramide at higher ceramide:lipid ratios (0.5), where

45 C2-ceramide, at concentrations which antagonized activat

46 An inhibitor of PLD activation, C2-ceramide, attenuated ET-1-induced PLD activity, as in

47 The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indi

48 tivation and degranulation were inhibited by C2-ceramide but not dihydro-C2-ceramide.

49 Results indicate that C2-ceramide but not inactive C2-dihydroceramide, was fou

50 cation of a cell permeable ceramide analogue C2 ceramide, but not the biologically inactive C2 dihydr

51 c7 cells also arrested following exposure to C2-ceramide, but did not undergo apoptosis.

52 area/anterior hypothalamic neurons show that C2-ceramide, but not dihydroceramide, mimics the rapid h

53 events apoptosis induced by camptothecin and C2-ceramide by phosphorylating BAD on Ser-112 in a prote

54 -permeable, short-chain ceramide analog, the C2-ceramide (C2-cer).

55 C2-Ceramide caused nearly total leakage of dye from the

56 re of 1c1c7 cultures to N-acetylsphingosine (C2-ceramide) caused a concentration-dependent inhibition

57 We report here that (1) exposure to C2-ceramide (cer) rarely increases OLG Cai, whereas sphi

58 rthermore, the inhibition of phagocytosis by C2-ceramide correlated with the inhibition of tyrosine p

59 alkaline hydrolysis, and ability to form the C2-ceramide dibenzoate derivative.

60 C2-ceramide did not inhibit insulin-stimulated phosphory

61 meabilized PMNs stimulated with GTP gamma S, C2-ceramide did not inhibit RhoA translocation.

62 Treating cells with C2-ceramide does not affect phosphorylation of insulin r

63 LPS-induced cell death and less sensitive to C2 ceramide-evoked cytotoxicity, when compared with Lps(

64 Unlike lipopolysaccharide, C2-ceramide failed to activate NF-kappaB and did not ind

65 ch as diacylglycerol, phosphatidic acid, and C2-ceramide, failed to induce a significant increase in

66 Pretreatment of C3H/OuJ macrophages with C2-ceramide greatly diminished AP-1 induction following

67 ontrast, N-acetyldihydrosphingosine (dihydro-C2-ceramide) had no effect on either tyrosine phosphoryl

68 Collectively, because C2-ceramide has many biological activities that differ f

69 eed in the absence of p53, exogenously added C2-ceramide increased the cellular p53 level in LM cells

70 C2-Ceramide induced a larger decrease in anisotropy than

71 cells, Fas ligation or addition of exogenous C2-ceramide induced activations of caspase-3/CPP32 and c

72 and its downstream substrates, and inhibits C2-ceramide induced apoptosis.

73 Synthetic cell permeable C2-ceramide induced apoptotic death of rat neonatal card

74 ted of c-Fos, Jun-B, Jun-D, and c-Jun, while C2-ceramide induced Jun-D and c-Jun only.

75 PS and the cell-permeable ceramide analogue, C2 ceramide, induced significant cell death in IFN-gamma

76 Notably, the drug rescued C2 ceramide-induced ER stress-mediated apoptosis and ER

77 tion of NF-kappaB and AP-1 but did not block C2-ceramide-induced AP-1.

78 ip between AHR content and susceptibility to C2-ceramide-induced apoptosis.

79 t constitutively active Akt kinase decreases C2-ceramide-induced death of HMN1 cells as well as COS-7

80 Importantly, C2-ceramide-induced suppression of calpain phosphorylati

81 Strikingly, C2 ceramide induces, whereas its phosphorylated derivati

82 Our data show that C2-ceramide induces apoptosis in HMN1 motor neuron cells

83 of studies, the short-chain ceramide analog C2-ceramide inhibited insulin-stimulated glucose transpo

84 Prior incubation of PMNs with 10 microM C2-ceramide inhibited PLD activity and RhoA translocatio

85 N-Acetylsphingosine (C2-ceramide) inhibited phagocytosis, reduced ERK1 and ER

86 fluidity of lipid vesicles all suggest that C2-ceramide inhibits platelet aggregation because it des

87 ramide did not induce lysis, suggesting that C2-ceramide is able to destabilize membranes.

88 C2-ceramide is produced via PAF:sphingosine transacetyla

89 Here, membrane permeant C2-ceramide is shown to attenuate the basal and insulin-

90 treated with D-erythro-MAPP prior to feeding C2 ceramide manifest markedly elevated levels of apoptos

91 Exogenous C2-ceramide markedly increased apoptosis in quiescent Ve

92 tment inhibited both lipopolysaccharide- and C2-ceramide-mediated responses.

93 thalamic application of the cell-penetrating C2-ceramide mimics the rapid phase of the IL-1beta-induc

94 The ceramide analog C2-ceramide (N-acetylsphingosine) was without effect on

95 This indicates that the effect of C2-ceramide on ADP-induced platelet aggregation depends

96 ase activity, suggesting that the effects of C2-ceramide on Akt kinase are not mediated through modul

97 of iNOS, we examined the effect of SMase and C2-ceramide on the activation of NF-kappaB.

98 Addition of exogenous C2 ceramide or bacterial-derived sphingomyelinase to alv

99 Moreover, we report that addition of C2-ceramide or D-erythrosphingosine to neutrophils after

100 Treatment with C2-ceramide or sphingomyelinase did not alter NF-ELAM1 s

101 Lipopolysaccharide and, less potently, C2-ceramide or sphingomyelinase, stimulated AP-1-depende

102 resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide).

103 is factor alpha (TNFalpha), antibody to Fas, C2-ceramide, osmotic shock (sorbitol), and thermal shock

104 C2 ceramide plus IFN-gamma failed to activate release of

105 ed the nonspecific effects on membranes that C2-ceramide possessed, suggesting that C2-dihydroceramid

106 dominant-negative FAN--expressing cells with C2-ceramide produced substantial cell death, indicating

107 ml(-1) NGF or 1 microM N-acetyl sphingosine (C2-ceramide) produced a 3- to 4-fold increase in the num

108 ine-phospholipase D (PC-PLD), butan-1-ol and C2 ceramide, produced marked inhibition of constitutive

109 atment, normal WI38 cells cleared 17% of [3H]C2-ceramide producing [3H]C2-SM, which accounted for 13%

110 ort that apoptotic stimuli (staurosporine or C2-ceramide) reciprocally altered Bcl-x splicing in neur

111 Moreover, non-toxic levels of exogenous C2-ceramide sensitized LNCaP cells to irradiation simila

112 C), etoposide, or sphingoid bases (including C2 ceramide, sphingosine, or sphinganine) caused the acc

113 xogenously-added sphingolipids (sphingosine, C2-ceramide, sphingosine 1-phosphate, and N,N-dimethylsp

114 hed by its identical Rf value with authentic C2-ceramide standard on thin-layer plate, sensitivity to

115 minished AP-1 induction following subsequent C2-ceramide stimulation.

116 by IL-1 beta differs from that activated by C2-ceramide, suggesting that signaling pathways utilized

117 However, apoptosis could be induced with C2-ceramide, suggesting that signals proximal to the gen

118 The ability of C2-ceramide to cause platelet fenestrations, formation o

119 The addition of [3H]C2-ceramide to cells resulted in a time-dependent format

120 or modulated the development of apoptosis in C2-ceramide-treated 1c1c7 cultures.

121 dissociate Bax from isolated mitochondria of C2-ceramide-treated cells.

122 ia were measured with fluorescent markers in C2-ceramide-treated primary cultures of mesencephalic ne

123 modes including tumor necrosis factor alpha, C2-ceramide, UV irradiation, and serum deprivation.

124 osis induced by tumor necrosis factor alpha, C2-ceramide, UV irradiation, or serum deprivation.

125 C2-ceramide was also unable to activate NF-kappaB, a tra

126 (n=166), and vascular reactivity to flow and C2-ceramide was assessed.

127 Furthermore, exogenous C2-ceramide was cytotoxic to bovine brain endothelial ce

128 des with short fatty acyl groups-d18:1-C2:0 (C2-ceramide, where d18:1 is sphingosine and C2:O is an a

129 8 cells by exposure of the cells to SMase or C2-ceramide, whereas phospholipase A2 or phospholipase C

130 Conversely, overexpression of Smpd3 or C2-ceramide, which mimics the function of nSMase2, inhib

131 respiratory chain complex III is reduced by C2-ceramide with half-maximum effect at 5-7 microM.

132 C2-Ceramide without FFA induced DNA laddering, but fumon