ライフサイエンスコーパス: DETA

1 DETA NONOate, a nitric oxide donor, inhibited the basal,

2 DETA-NO also decreased NF-kappaB DNA binding activity an

3 DETA-NO generated nitric oxide (as indicated by an incre

4 DETA-NONOate (1 mM) produced a steady-state concentratio

5 DETA-NONOate (1 mM), which releases NO in the range prod

6 DETA-NONOate, a long acting NO donor which has a half-li

7 DETA-NONOate, a long acting NO donor, with a half-life o

8 DETA-NONOate, a nitric oxide (NO) donor, induced cytosta

9 111In-DOTA-MA), or 99mTc (FBP16, 99mTc(CO)3-DETA-PA), respectively.

10 f the glass and cantilever substrates with a DETA SAM, a serum-free medium and refined culture techni

11 lamine (SNAP), diethylenetriamine NO adduct (DETA-NO), and sodium nitroprusside provide (SNP), were f

12 nor, diethylenetriamine nitric oxide adduct (DETA-NO), promotes cell survival.

13 O donor diethyleneamine/nitric oxide adduct (DETA-NO).

14 -2% after SNAP (P<0.05) and to 85+/-1% after DETA/NO (P<0.05).

15 NAP (group IV) (P<0.05) and to 52+/-2% after DETA/NO (group V) (P<0.05).

16 on of several cell signaling molecules after DETA-NO preconditioning was observed by Western blotting

17 cell death induced by oxidative stress after DETA-NO preconditioning; this cytoprotective effect was

18 By gel mobility shift analysis, DETA-NO inhibited TNF-alpha activation of DNA binding pr

19 but not to sodium nitroprusside, SIN-1, and DETA-NO.

20 In this study, NO donors (SNAP and DETA-NONOate) inhibited DC antigen presentation.

21 Thus, the effects of SNAP and DETA/NO on PKC closely resembled those of ischemic PC.

22 suggest a functional sGC heterodimer because DETA-NO increased cGMP levels in low-passage human and p

23 tion of the concentration of NO generated by DETA/NO, with N. gonorrhoeae reducing the NO from proinf

24 ed by oxidized LDL, and LPS was inhibited by DETA-NO.

25 prevented upregulation of PGC-1alpha mRNA by DETA-NO.

26 that down-regulation of cyclin D1 protein by DETA-NONOate played an important role in the cytostasis

27 Using thin layer chromatography, DETA-NO (100 microM) suppressed formation of this metabo

28 (trimethoxysilyl)propyl] diethylenetriamine (DETA) and fabricated microcantilevers to promote the dif

29 ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO), and the NO synthase inhibitor, NG-monomethyl-L

30 onioethyl) aminio] diazen-1-ium-1,2-diolate (DETA/NONOate), enhances angiogenesis, neurogenesis and n

31 monioethyl) aminio]diazen-1-ium-1,2-diolate (DETA/NONOate), to young adult rats significantly increas

32 mmonioethyl)amino]diazen-1- ium-1,2-diolate [DETA-NO]) or block nitric oxide production (Nomega-methy

33 ion of ICAM-1 mutant cells with the NO donor DETA NONOate (0.1 microM) corrected the migration defect

34 The NO donor DETA-NO increased ecSOD expression in a time- and dose-d

35 Incubation with the NO donor DETA-NO inhibited VIC osteogenic differentiation and mat

36 In this study, we used the NO donor DETA-NO to model NO exposure to cervical epithelium.

37 revious exposure of the SMCs to the NO donor DETA-NONOate (100 micromol/L) (P<.05).

38 We used the long-acting NO donor DETA-NONOate, which, at a concentration of 1 mM, release

39 When the NO donor DETA/NO was used to simulate host NO production, N. gono

40 Low concentrations of the NO donor, DETA NONOate (<200 microM), exclusively nitrate Tyr327 w

41 ot mimic the effects of nitric oxide donors (DETA-NO) on apoptosis.

42 ,2'-(hydroxynitrosohydrazino)bis-ethanamine (DETA/NONOate) had a bacteriostatic effect on C. burnetii

43 NNA and its agonist scutellarin, hemoglobin, DETA/NO (nitric oxide(NO) donor), PITO (NO scavenger), 8

44 edia, 24-hour exposure to 0.25 to 0.5 mmol/L DETA-NO yielded a pathologically relevant NO concentrati

45 e (DOTA-MA), or a diethylenetriamine ligand (DETA-propanoic acid [PA]), followed by labeling with 68G

46 Moreover, DETA-NO suppressed TNF-alpha-induced mRNA accumulation o

47 thelial cells, the NO donor diethylamine-NO (DETA-NO, 100 microM) reduced VCAM-1 gene expression indu

48 ent with an NO donor: diethylenetriamine-NO (DETA-NO).

49 y giving the NO donor diethylenetriamine/NO (DETA/NO) (at a dose previously shown to elicit late PC),

50 unrelated NO donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at

51 e given the NO donors diethylenetriamine/NO (DETA/NO, 0.1 mg/kg i.v., 4 times [group II, n=5]) or S-n

52 e (SNAP, 25 muM) or diethylenetriamine-NONO (DETA-NO, 50 muM), exhibited elevated AMPK phosphorylatio

53 with 100 microm diethylenetriamine NONOate (DETA NONOate) for 24-96 h decreased both intracellular a

54 thione (GSNO) or diethylenetriamine NONOate (DETA NONOate).

55 ium-1,2-diolate (diethylenetriamine NONOate, DETA-NO) (1 mmol/liter) under normoxic or hypoxic condit

56 tely abrogated the infarct-sparing action of DETA/NO (group X, n=7).

57 Administration of DETA/NONOate significantly increases cortical levels of

58 Furthermore, administration of DETA/NONOate to rats subjected to embolic middle cerebra

59 cells with 1,25D and a low-concentration of DETA NONOate led to a significant decrease in the overal

60 In fact, high concentrations of DETA-NO were found to inhibit MMP-9 activity, presumably

61 tiated the action of lower concentrations of DETA-NONOate (25-100 microM) by inducing apoptosis in th

62 uld not be increased by doubling the dose of DETA/NO (group VIII, n=5).

63 r cGMP in mediating the protective effect of DETA-NO in our model.

64 ssion did not alter the protective effect of DETA-NO on cell survival.

65 The protective effect of DETA/NO was completely abrogated when this agent was giv

66 n cyclin D1 was reversible for up to 48 h of DETA-NONOate (1 mM) treatment.

67 membrane potential (MMP) occurred at 4 h of DETA-NONOate treatment, which returned to control values

68 d 50% decrease in the levels pAkt at 24 h of DETA-NONOate treatment.

69 evels of cytosolic phospho-Akt at 16-24 h of DETA-NONOate treatment.

70 However, the inability of DETA-NO to cause increases in cGMP levels in transformed

71 Ceramide had no effect on DETA NONOate-induced vasodilation.

72 (GSNO) or the NONOates, DEA-NO, SPER-NO, or DETA-NO, were ineffective.

73 Furthermore, we observed that DETA-NO promotes mitochondrial biogenesis and elongation

74 ormation of this metabolite, suggesting that DETA-NO modifies the reactivity of oxygen intermediates

75 The DETA/NO-induced translocation of PKCepsilon (but not tha

76 se of chelerythrine completely prevented the DETA/NO-induced late PC effect against both myocardial s

77 Exposure of SC cells to DETA-NO resulted in a 12% to 16% decrease in cell volume

78 chronized population of the cells exposed to DETA-NONOate remained arrested at the G(1) phase of the

79 Exposure to DETA-NO resulted in a decrease in Psim and concomitant r

80 Exposure to DETA-NO resulted in increased sIPSCs and mIPSCs frequenc

81 t of H-Ras transformed HMLE(HRas) cells with DETA NONOate, a nitric oxide (NO)-donor led to induction

82 Thus, preconditioning hCSCs with DETA-NO promotes cell survival and resistance to oxidati

83 se tracheal epithelial cells, incubated with DETA NONOate but not with 100 microm 8-bromo-cGMP for 96

84 of cell adhesion molecules was observed with DETA alone.

85 When rabbits were pretreated with DETA/NO (group VII, n=8) or SNAP (group IX, n=7) 24 hour

86 BAEC treated with DETA-NO under normoxic conditions demonstrated increased

87 Treatment with DETA/ NONOate also increases neurogenesis in the dentate