ライフサイエンスコーパス: dinitrophenol

1 nilyl) and at the other end with a quencher (dinitrophenol).

2 pylamine incorporation, visualized with anti-dinitrophenol.

3 and removal of the mitochondrial poison 2,4 dinitrophenol.

4 opy of subunits complexed with antibodies to dinitrophenol.

5 6.5, not at pH 8.0, and were not induced by dinitrophenol.

6 se matched proteins induced by the uncoupler dinitrophenol.

7 pleted of energy with 2-deoxyglucose and 2,4-dinitrophenol.

8 is very much larger than that of 2,4- or 2,5-dinitrophenol (0.09 and 0.11), indicating a very much re

9 The hydrogen bond acidity of 2,3-dinitrophenol (0.67) is very much larger than that of 2,

10 luoromethoxy-phenylhydrazone (1-3 nM) or 2,4-dinitrophenol (100 nM) significantly antagonized and del

11 the genes involved in the degradation of 2,4-dinitrophenol (2,4-DNP) in a Rhodococcus erythropolis st

12 The separation of 4-nitrophenol, 2,4-dinitrophenol, 2-methyl-4-nitrophenol, 3-methyl-4-nitrop

13 the inhibitors, conduritol beta-epoxide and dinitrophenol-2-deoxy-2-fluoro-beta-D-glucopyranoside (D

14 environment on the rate of photolysis of 2,4-dinitrophenol (24-DNP), an important environmental toxin

15 yanide m-chlorophenylhydrazone, 44%, and 2,4-dinitrophenol, 26%), by sodium azide (25%), and hydroxyl

16 benzene (1.0 +/- 0.7) x 10(6) M(-1); and 2,4-dinitrophenol (5.1 +/- 3.0) x 10(4) M(-1).

17 on of HTC hepatoma cells by exposure to 2, 4-dinitrophenol (50 microM) and 2-deoxy-D-glucose (10 mM)

18 Cells were exposed to dinitrophenol (50 microM) and 2-deoxyglucose (10 mM) as

19 ilar but much smaller effect occurs with 2,6-dinitrophenol (A = 0.17).

20 e (AICAR), rotenone (a Complex I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contra

21 For instance, aqueous 2,4-dinitrophenol absorption varies dramatically over the pH

22 growth conditions in the presence of 0.1 mM dinitrophenol, an uncoupler of ATP synthesis.

23 somes is ATP-dependent, and ATP depletion by dinitrophenol and 2-deoxyglucose also inhibited apoB deg

24 io calculations which show that 2,3- and 2,6-dinitrophenol and picric acid are significantly distorte

25 The dinitrophenols and picric acid are similarly discussed.

26 nic acid), electrophilic substrate analogue (dinitrophenol), and product analogues (S-hexylglutathion

27 ropic agent chloroquine, the energy depleter dinitrophenol, and also by low temperature, suggesting t

28 m: carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5 killing of Cand

29 Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5-induced ATP eff

30 cell lines or colonic biopsy specimens using dinitrophenol, and barrier function was assessed by tran

31 ated that sodium salicylate, plumbagin, 2, 4-dinitrophenol, and menadione-inducers of the marRAB oper

32 arbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophenol, and nigericin but not by the potassium io

33 -hydroxy-2-nonenal (HNE) -modified proteins, dinitrophenol, and nitrotyrosine to quantify and localiz

34 amino acid secretions was verified using 2,4-dinitrophenol as an inhibitor of the proton motive force

35 2-aminobenzyl-GGFLRKVGQ-ethylenediamine-2,4-dinitrophenol at the R-K bond, exhibiting a K(m) of 13 m

36 A mitochondrial uncoupler, 2,4-dinitrophenol (at 1 mmol/L), blocked the effects of 8-Br

37 ress and the mitochondrial uncoupling agent, dinitrophenol, both of which lead to increased glucose t

38 yanide m-chlorophenylhydrazone) and DNP (2,4-dinitrophenol) but completely inhibited by cyanide.

39 ol C6H5NO4, methylnitrocatechol C7H7NO4, and dinitrophenol C6H4N2O5) measured with a micro-orifice vo

40 of these cells by macrophages; and (3) that dinitrophenol can be used as a surrogate for quantitatin

41 bind putative ligands of the EmrAB pump-2,4-dinitrophenol, carbonyl cyanide m-chlorophenylhydrazone,

42 ing of a haptenated fluorescent protein, 2,4-dinitrophenol-coupled B-phycoerythrin (DNP25-PE), to flu

43 Both 2,4-dinitrophenol (DNP) and carbonyl cyanide p-trifluorometh

44 e observed with the metabolic inhibitors 2,4-dinitrophenol (DNP) and sodium azide.

45 A23187 and the mitochondrial uncoupler, 2,4-dinitrophenol (DNP) as damaging agents.

46 n be quenched by both the negatively charged dinitrophenol (DNP) derivative, (DNP-BS(-)), and positiv

47 The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effects on NAFLD, ins

48 on of the mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) in a large animal model with minimum

49 efficacy of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) in animals receiving striatal inject

50 Metformin increased PCr recovery from either dinitrophenol (DNP) or azide in L6 cells.

51 vical spinal cord transection, NaCN and also dinitrophenol (DNP) significantly (P < 0.05) elevated rC

52 od are demonstrated using the binding of 2,4-dinitrophenol (DNP) to transthyretin (TTR), as well as p

53 The chemical uncoupler 2,4-dinitrophenol (DNP) was an effective and widely used wei

54 the presence of the mitochondrial uncoupler dinitrophenol (DNP) were compared using 16.4 T in isoflu

55 onyl cyanide m-chlorophenylhydrazone (CCCP), dinitrophenol (DNP), or CN(-), resulted in massive disso

56 of increased UCP3 expression), and acute 2,4-dinitrophenol (DNP)-treated (protonophore and mitochondr

57 s was induced by addition and removal of 2,4-dinitrophenol (DNP).

58 ole-cell recordings, bath application of 2,4-dinitrophenol (DNP, an uncoupler of mitochondrial ATP pr

59 CsA, 42.6+/-9.0% with SfA; P<0.001), or 2,4-dinitrophenol (DNP, the mitochondrial uncoupler, 50 micr

60 Mitochondrial superoxide evoked by dinitrophenol elicited significant internalization and t

61 -N-oxide and 2-[1-(p-chlorophenyl)ethyl] 4,6-dinitrophenol establish that both inhibitors block the b

62 e heat shock response, including salicylate, dinitrophenol, ethanol, and arsenite, have no effect on

63 disease, and the mitochondrial uncoupler 2,4-dinitrophenol for obesity.

64 PH), a primary antibody specific for the 2,4-dinitrophenol group, and a peroxidase-labeled second ant

65 AMPK activator dinitrophenol had effects on ERK, aPKCs, and 2-DOG uptak

66 ans blue dye in mice passively sensitized to dinitrophenol-human serum albumin and challenged intrade

67 so studied in mice passively sensitized with dinitrophenol-human serum albumin and challenged intrade

68 ctivation by the lipophilic protonophore 2-4 dinitrophenol in a pH-dependent manner.

69 onstant for 3 hours and that exposure to 2,4-dinitrophenol increased QO2.

70 We have previously reported that 2-alkyl-4,6-dinitrophenols inhibit mammalian complexes I, II, and II

71 ide-4-(trifluoromethoxy) phenylhydrazone and dinitrophenol inhibited inositol transport by 50-70% in

72 nide-4-(trifluoromethoxy)phenylhydrazone and dinitrophenol inhibited inositol transport by 50-70% in

73 of the substituent in the 2-position of the dinitrophenol inhibitors.

74 stearoyl-oleoyl-phosphatidylcholine plus 3% dinitrophenol-linked di-oleoyl-phosphatidylethanolamine.

75 lic cation and releases the protonophore 2,4-dinitrophenol locally in predetermined regions in respon

76 One millimolar 2,4-dinitrophenol lowered the ATP in wild type to that in th

77 e protective effect of pretreatment with 2,4-dinitrophenol, measured from increased functional recove

78 tion by 150 microM GS-Succ-BP is provided by dinitrophenol, nitrobenzene, ethacrynic acid, and S-hexy

79 n in residue H19 impaired the binding to 2,4-dinitrophenol only.

80 Out of six possible positional isomers of dinitrophenol, only 2,4-DNP has been used extensively by

81 inhibitors of ATP synthesis (oligomycin, 2,4-dinitrophenol, or 2-deoxyglucose) made them more suscept

82 Strophanthidin inhibits KATP channels in 2,4-dinitrophenol-poisoned heart cells ().

83 Addition of the metabolic poisons cyanide or dinitrophenol reduced the active transport of both prote

84 A showed that there was a rapid burst of 2,4-dinitrophenol release.

85 pleted by treatment with sodium azide or 2,4-dinitrophenol; restoration of the original ATP levels oc

86 The uncouplers S13 and dinitrophenol showed that NarK2 was not dependent on the

87 Transport was also inhibited by 2,4-dinitrophenol, suggesting an energy-linked transport mec

88 l assays for the environmental pollutant 2,4-dinitrophenol the alternative devices were 50% more sens

89 rs with very good leaving groups such as 2,4-dinitrophenol, the monoanion of phosphate esters is more

90 Treatment of the FF group with low dose 2,4-dinitrophenol to increase energy expenditure abrogated t

91 ation of mitochondria in the presence of 2,4-dinitrophenol uncoupler.

92 ies we have selected a series of 2-alkyl-4,6-dinitrophenols which proved to be very effective noncomp

93 y reduced binding to both salicylate and 2,4-dinitrophenol, while a mutation in residue H19 impaired