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 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