ライフサイエンスコーパス: DFP

1 DFP 1 mg/mL in drinking water increased retinal Tfrc mRN

2 DFP at 60 muM decreased labile iron in ARPE-19 cells, in

3 DFP exposure elicited comparable effects on phosphorylat

4 DFP formation (Kcat and kcat/Km), DFP decay, and protein

5 DFP treated rats, exhibited significantly reduced expres

6 DFP treatment significantly altered phosphorylation at r

7 DFP was not retina toxic in wild-type (WT) or DKO mice,

8 [3H]DFP labeling of chymotrypsin was suppressed by both BAEE

9 [3H]DFP reacted with brain microsomes to produce nine distin

10 t with [3H]diisopropylphosphofluoridate ([3H]DFP) to produce radioactive adducts that can be resolved

11 tol deacylase was affinity labelled with [3H]DFP and purified.

12 Trypsin labeling with [3H]DFP was suppressed by alpha-N-benzoyl-l-arginine ethyl e

13 ould suppress the enzyme's reaction with [3H]DFP.

14 ith the laminin-derived peptide EFPDFP and a DFP peptide from the random screen demonstrated binding

15 ed phase of learning impairment to sub-acute DFP exposure, which may involve the loss of hippocampal

16 A better tolerance to AN-238 after DFP treatment is due to the selective uptake of AN-238 b

17 amide caused large decreases in firing after DFP, confirming sustained ACh release.

18 ylation was bi-directionally regulated after DFP in striatum versus hippocampus.

19 ent complications but safely protect against DFP-induced seizures and other CNS toxicity, we adopted

20 Da for the active site peptide peak of aged DFP-inhibited NEST, corresponding to a monoisopropyl pho

21 parathion, and dimefox, and the nerve agents DFP, tabun, sarin, cyclosarin, soman, VX, and Russian-VX

22 ins by the brain supernatants of control and DFP-treated hens.

23 Both neostigmine and DFP applied after AChE inhibition by DFP sometimes elici

24 e DFP) with IMI (2 mg/kg s.c., 30 min before DFP) prevents DFP-induced convulsions and the associated

25 ion of HUP (50 microg/kg s.c., 15 min before DFP) with IMI (2 mg/kg s.c., 30 min before DFP) prevents

26 l change to a final level higher than before DFP.

27 -pretreated mice, the ED(50) of IMI to block DFP-induced mortality is approximately 10 times lower th

28 served changes in phosphorylation induced by DFP.

29 drolysis of polar PC, which was inhibited by DFP.

30 ine and DFP applied after AChE inhibition by DFP sometimes elicited a transient response.

31 The rate of inactivation of rh-PSA by DFP is 30-fold faster in the presence of 0.9 M Na(2)SO(4

32 axis with pyridostigmine bromide (PB) caused DFP-treated animals to exhibit near normal levels of mem

33 In contrast, DFP has no effect on the tolerance of AN-201.

34 ction by the oral iron chelator deferiprone (DFP).

35 he 3 drugs, deferoxamine (DFO), deferiprone (DFP), and deferasirox (DFX), including their efficacy, p

36 are inhibited by diisopropylfluorophosphate (DFP).

37 xon, dichlorvos, diisopropylfluorophosphate (DFP), and sarin covalently bind to human albumin.

38 other hand, 1 mM diisopropylfluorophosphate (DFP) completely inhibited LCAT but had no effect on PAF-

39 os oxon (CPO) or diisopropylfluorophosphate (DFP): human serum albumin (K212, K414, K199, and K351),

40 amidine (pAB) and diisopropylfluorphosphate (DFP) were impaired 1.6-36-fold and 35-478-fold, respecti

41 (AChE) inhibitor, diisopropylflurophosphate (DFP) were administered as single daily injections concom

42 dition, low level diisopropylflurophosphate (DFP) exposure (0.25 mg/kg per day for 2 weeks) in rats r

43 Diisopropylphosphorofluoridate (DFP), the oxygen analogue of MIP, was used for compariso

44 In DKOs, DFP over 8 months decreased retinal iron levels to 72% o

45 Diisopropyl fluorophosphate (DFP) causes neurotoxicity related to an irreversible inh

46 groups such as diisopropyl fluorophosphate (DFP) or venomous agent X, creating a major challenge for

47 AChE inhibitor diisopropyl fluorophosphate (DFP) usually caused a sustained increase, with an initia

48 Diisopropyl fluorophosphate (DFP) was used as a nerve gas mimic.

49 a CE inhibitor, diisopropyl fluorophosphate (DFP), to mouse serum in vitro significantly (P < 0.01) p

50 he OP compound, diisopropyl fluorophosphate (DFP).

51 phate substrate diisopropyl fluorophosphate (DFP).

52 d with inactive diisopropyl-fluorophosphate [DFP]-thrombin) and mediated via the protease-activated r

53 complex with diisopropyl fluorophosphonate (DFP, a potent serine hydrolase inhibitor) were determine

54 n, anti-PRCP, diisopropyl-fluorophosphonate (DFP), phenylmethylsulfonyl fluoride (PMSF), and Z-Pro-Pr

55 5 and 1938 for dichlorvos, 1881 and 1994 for DFP, and 1838 and 1938 for sarin; these masses fit a mec

56 The detection limit for DFP is 2 x 10(-6) M with a potential drop between 40 and

57 Characteristic fragments specific for DFP-labeled lysine appeared at 164.0, 181.2, and 83.8amu

58 Kinetic values for DFP against NEST were as follows: k(i) = 17 200 +/- 180

59 Brain supernatants from DFP-treated hens showed enhanced in vitro phosphorylatio

60 The [(3)H]DFP-labeled protease was detected as three protein bands

61 PON1 prevent it from being able to hydrolyze DFP with its fluoride leaving group.

62 F subunits in the cytoskeletal inclusions in DFP-treated hen spinal cord cross-sections.

63 r piroxicam or the selective COX-2 inhibitor DFP, but by inhibitors of either secretory or cytosolic

64 that when the acetylcholinesterase inhibitor DFP was co-administered with morphine, both the increase

65 DFP formation (Kcat and kcat/Km), DFP decay, and protein-caged hydrated ferric oxide accum

66 Pefabloc and by 30% in the presence of 1 mM DFP.

67 rent mechanism in the axonal aggregations of DFP-treated hen.

68 The binding of DFP to Tyr411 of human albumin was confirmed by electros

69 lation state of phosphoproteins in brains of DFP-treated mice; hippocampus and striatum were analyzed

70 filament (NF) subunits in the spinal cord of DFP-treated hens.

71 chiometry of NF-M:NF-L in the spinal cord of DFP-treated hens.

72 A single dose of DFP (1.7 mg/kg, s.c.) produces mild ataxia in 7-14 days

73 A single dose of DFP (1.7 mg/kg, sc.) produces mild ataxia in 7-14 days i

74 Hens were treated with a single dose of DFP and sacrificed 1, 5, 10, and 20 days post-treatment.

75 We studied the effect of DFP administration on Ca2+/calmodulin-dependent phosphor

76 The apparent anti-withdrawal effect of DFP was not reproduced by the selective peripherally act

77 These changes were observed within 24 h of DFP administration and persisted for 10-20 days.

78 with time due to the catalyzed hydrolysis of DFP and the production of fluoride ion.

79 In the presence of DFP, the electrode potential decreases rapidly with time

80 tion of tau proteins by brain supernatant of DFP-treated hens that includes phosphorylation of a numb

81 Further testing of DFP for retinal disease involving oxidative stress is wa

82 The use of DFP together with these peptide conjugates in nude mice

83 Oral DFP was not toxic to the mouse retina.

84 t, and safe therapeutic strategy to overcome DFP toxicity.

85 93 is deleterious for interactions with pAB, DFP and amidolytic substrates, situations where no S2'-P

86 ubstrates are coupled via a diferric peroxo (DFP) intermediate, lambdamax 650 nm, which decays to [Fe

87 Diisopropyl phosphofluoridate (DFP) at high concentration partially inhibited the prote

88 Diisopropyl phosphorofluoridate (DFP) is an organophosphorus ester, which produces organo

89 Diisopropyl phosphorofluoridate (DFP) produces organophosphorus ester-induced delayed neu

90 I (2 mg/kg s.c., 30 min before DFP) prevents DFP-induced convulsions and the associated neuronal dama

91 motifs containing the signature Asp-Phe-Pro (DFP) tripeptide.

92 ith its monocyte chemotactic activity, since DFP- or PMSF-inactivated cathepsin G no longer induced m

93 the rate of endogenous ACh release, and that DFP and reversible AChE inhibitors exert an initial tran

94 to show a temporal relationship between the DFP-induced impairment in performance of a spatial memor

95 domain, and central to the interaction, the DFP phenylalanine side-chain inserts into a major hydrop

96 This revealed the location of the DFP peptide bound to the FXI apple 2 domain, and central

97 icotine was shown to completely reverse this DFP-induced impairment in memory-related task performanc

98 lude that the level of sustained response to DFP is determined by the rate of endogenous ACh release,

99 When DFP is used in vivo, 400 nmol/kg cytotoxic somatostatin

100 as attenuated when Lp(a) was pretreated with DFP suggesting that the serine residue in the pseudo act

101 l (ARPE-19) cells and mice were treated with DFP.

102 all animals die after the same dose without DFP.