ライフサイエンスコーパス: dinitrobenzene

1 covered and designated ROD1 (resistance to o-dinitrobenzene).

2 nzyme's preferred substrate is 1-chloro-2, 4-dinitrobenzene.

3 glutathione sulfonic acid, and glutathione-s-dinitrobenzene.

4 to discriminate between the three isomers of dinitrobenzene.

5 esized bearing 1 to 4 sulfonamide-linked 2,4-dinitrobenzene.

6 ding unique responses for dinitrotoluene and dinitrobenzene.

7 ect transferase activity toward 1-chloro-2,4-dinitrobenzene.

8 xed saturating concentration of 1-chloro-2,4-dinitrobenzene.

9 rom that of monobromobimane and 1-chloro-2,4 dinitrobenzene.

10 elated to substrates, including 1-chloro-2,4-dinitrobenzene.

11 ted by the GSH-specific reagent 1-chloro-2,4-dinitrobenzene.

12 -1 for the native enzyme toward 1-chloro-2,4-dinitrobenzene.

13 The electrochemistry of 1,2-dinitrobenzene (1,2-DNB), 1,3-dinitrobenzene (1,3-DNB),

14 Normalized response profiles for 1,3-dinitrobenzene (1,3-DNB) are independent of analyte conc

15 emistry of 1,2-dinitrobenzene (1,2-DNB), 1,3-dinitrobenzene (1,3-DNB), and 1,4-dinitrobenzene (1,4-DN

16 -DNB), 1,3-dinitrobenzene (1,3-DNB), and 1,4-dinitrobenzene (1,4-DNB) is strongly affected by the pre

17 itrotoluene (7.9 +/- 4.0) x 10(6) M(-1); 1,3-dinitrobenzene (1.0 +/- 0.7) x 10(6) M(-1); and 2,4-dini

18 xide diamine (HMTD), 2,4-dinitrotoluene, 1,3-dinitrobenzene, 1,3,5-trinitrobenzene, 2-amino-4,6-dinit

19 dinitroaromatic radical anions (1,2- and 1,4-dinitrobenzene, 1,5- and 2,6-dinitro naphthalene, 4,4'-d

20 ocalized) intervalence radical anions of 1,4-dinitrobenzene, 2,6-dinitronaphthalene, 2,6-dinitroanthr

21 inity peptide tag, (64)Cu-L19K-(5-fluoro-2,4-dinitrobenzene) ((64)Cu-L19K-FDNB), which binds covalent

22 ddition of glutathione (GSH) to 1-chloro-2,4-dinitrobenzene, a reaction in which the chemical step is

23 eater than marginal activity with chloro-2,4 dinitrobenzene activity also exhibited significant activ

24 Cells treated with 1-chloro-2,4-dinitrobenzene, an irreversible inhibitor of thioredoxin

25 response is obtained for the explosives 1,3-dinitrobenzene and 2,4-dinitrotoluene over the 200-1,400

26 emically distinct sensitizers; 1-fluoro-2, 4-dinitrobenzene and 2-deoxyurushiol.

27 th 92% residual activity toward 1-chloro-2,4-dinitrobenzene and completely blocks Cys111 from subsequ

28 appreciable changes in K(m) for 1-chloro-2,4-dinitrobenzene and have similar CD spectra to that of wi

29 omatic compounds (1,3,5 trinitrobenzene, 1,3 dinitrobenzene, and 2,4 dinitrotoluene) and electronic s

30 a12,14-prostaglandin-J2, menadione, 1-Cl-2,4-dinitrobenzene, and biotinylated iodoacetamide.

31 cal inhibitor of Trx reductase, 1-chloro-2,4-dinitrobenzene, and Trx1 siRNA.

32 ith CuCN x 2LiBr and then oxidizing with 1,3-dinitrobenzene, and was used in a diversity-oriented syn

33 25 M(-1) s(-1)) compared to that of the 1,2-dinitrobenzene ( approximately 5 M(-1) s(-1)), whereas t

34 ic substrate sites (such as for 1-chloro-2,4-dinitrobenzene) are predominantly located within each su

35 With 1-chloro-2, 4-dinitrobenzene as a substrate, the His107 residue primar

36 tt2p exhibit GST activity with 1-chloro-2, 4-dinitrobenzene as a substrate.

37 nits/mg of cytosolic protein, using 1-Cl-2,4-dinitrobenzene as substrate), resulted in 70-90% reducti

38 tivities toward dimethenamid or 1-chloro-2,4-dinitrobenzene as substrates and in their levels of indu

39 enzyme was highly active toward 1-chloro-2,4-dinitrobenzene, as well as chloroacetanilide herbicides.

40 uctase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H(2)O(2) removal rates in mit

41 ncrease in GST activity toward 1-chloro-2, 4-dinitrobenzene but GST activity toward 4-HNE was increas

42 1,5-Bis-(dihexyl-N-nitrosoamino)-2,4-dinitrobenzene (C6') and an inactive form of the compoun

43 of the compound [1,5-bis-(dihexylamino)-2,4-dinitrobenzene (C6)] were tested in neuronal cell cultur

44 ls of enzymatic activity toward 1-chloro-2,4-dinitrobenzene (CDNB) and HNE were present in normal ste

45 is based on competition between 1-chloro-2,4-dinitrobenzene (CDNB) and the drugs for the GST enzyme i

46 exhibited high activity with 1-chloro-2, 4, dinitrobenzene (CDNB) but low activity with the chloroac

47 eaction between glutathione and 1-chloro-2,4-dinitrobenzene (CDNB) is widely used as a standard activ

48 When the general substrate 1-chloro-2-4-dinitrobenzene (CDNB) was used to assess GST activity wi

49 ly) the canonical GST substrate 1-chloro-2,4-dinitrobenzene (CDNB), and bear a wide variety of bioort

50 mmonly used synthetic substrate 1-chloro-2,4-dinitrobenzene (CDNB), but has relatively high glutathio

51 1-Chloro-2,4-dinitrobenzene (CDNB), which causes oxidative stress thr

52 in the crystal between GSH and 1-chloro-2,4-dinitrobenzene (CDNB).

53 with respect to turnover with 1-chloro-2, 4-dinitrobenzene (CDNB).

54 GSH but not for the cosubstrate 1-chloro-2,4-dinitrobenzene (CDNB).

55 hionine S,R-sulfoximine (BSO); 1-chloro, 2,4-dinitrobenzene (CDNB); or 1,3-bis (2-chloroethyl)-1-nitr

56 porter gene to screen a 1,5-dialkylamino-2,4-dinitrobenzene combinatorial chemical library consisting

57 The 1-fluoro-2,4-dinitrobenzene-conjugated dendritic cells that had been

58 P70 produced a reduction in the 1-fluoro-2,4-dinitrobenzene contact hypersensitivity response and res

59 pi-pi EDA interactions of dinitrobenzene contribute -17 to -19 kJ/mol (3-3.4 log u

60 droxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2

61 pproximately 5 M(-1) s(-1)), whereas the 1,4-dinitrobenzene did not show any proton transfer effect i

62 Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic

63 The location of the dinitrobenzene (DNB) ring in the GSDNB-GSTM2-2 complex w

64 rinitrobenzene (TNB), trinitrotoluene (TNT), dinitrobenzene (DNB), tetryl, and 2,4-dinitrotoluene (2,

65 he redox potentials of compounds such as 1,4-dinitrobenzene (DNB), which can be reduced in two one-el

66 roteins as a function of sensitivity to 1, 3-dinitrobenzene (DNB)-induced mitochondrial permeability

67 respect to their response to the toxicant m-dinitrobenzene (DNB).

68 carboxylic acid electron acceptors including dinitrobenzenes (DNBs) and naphthalenediimide (NI), whic

69 or the Trx reductase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB), in embryonic rat heart (H9c2) cel

70 Chronic application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to

71 AN9 toward the common substrate 1-chloro 2,4-dinitrobenzene, equilibrium dialysis, and tryptophan que

72 s more than 50-fold greater for 1-fluoro-2,4-dinitrobenzene (FDNB), and the product is the same for b

73 trate-dependent; in contrast to 1-chloro-2,4-dinitrobenzene, for the nucleophilic addition reaction o

74 nated peptide ions and radical anions of 1,3-dinitrobenzene formed exclusively c- and z-type fragment

75 ed sorption of benzene, naphthalene, and 1,4-dinitrobenzene from water to a series of wood chars made

76 hGSTM1a-1a complexed with 1-glutathionyl-2,4-dinitrobenzene (GS-DNB) formed by a reaction in the crys

77 nto DTY167 cells alleviates the 1-chloro-2,4-dinitrobenzene-hypersensitive phenotype concomitant with

78 active site alters affinity for 1-chloro-2,4-dinitrobenzene in the active site of the other subunit.

79 red forms by potassium-mirror reduction of p-dinitrobenzene in the presence of macrocyclic polyether

80 catalyze conjugation of GSH to 1-chloro-2,4-dinitrobenzene, indicating an absence of microsomal glut

81 tely inhibited activity toward 1-chloro-2, 4-dinitrobenzene, indicating that AFB-GSH binding to one a

82 t release is rate-limiting when 1-chloro-2,4-dinitrobenzene is the substrate.

83 In particular, the 1,3-dinitrobenzene isomer showed a higher proton transfer ra

84 d of electrogenerated dianionic species from dinitrobenzene isomers and substituted dihomooxacalix[4]

85 the complete discrimination of very similar dinitrobenzene isomers and three halogenated, substitute

86 Both mutants handle substrate 1-chloro-2,4-dinitrobenzene normally; however, Y103S exhibits a 30-fo

87 ein that is induced when the GST substrate o-dinitrobenzene (o-DNB) is added to the culture.

88 plosives-related compounds nitrobenzene, 1,3-dinitrobenzene, o-nitrotoluene, 2,4-dinitrotoluene, and

89 oluene, 2,6-dinitrotoluene, trinitrobenzene, dinitrobenzene, or 1,3,5-trinitro-1,3,5-triazacyclohexan

90 -transfer rates for the potassium salts of p-dinitrobenzene radical anion (DNB(-)).

91 ar unsymmetrical gas-phase structure for 1,3-dinitrobenzene radical anion but give serious spin conta

92 romyces cerevisiae leads to an increase in o-dinitrobenzene resistance in S. cerevisiae cells.

93 thione (GSH), by treatment with 1-chloro-2,4-dinitrobenzene, resulted in increased dense cells.

94 control, L19K was conjugated to 1-fluoro-2,4-dinitrobenzene, resulting in L19K-DNP.

95 dynein and myosin V using 1,5-difluoro-2, 4-dinitrobenzene revealed that this light chain exists as

96 n as that of the enzyme-GSH complex, and the dinitrobenzene ring is anchored between the side chains

97 minobenzoic acid substituent is bound to the dinitrobenzene ring via its carboxyl oxygen while the ot

98 nin-specific TH1 clone) or with 5S8 T cells (dinitrobenzene sulfonate specific Th0 clone) in the pres

99 induced with dextran sulfate sodium (DSS) or dinitrobenzene sulfonic acid (DNBS) in mice treated with

100 e mice significantly reduced the severity of dinitrobenzene sulfonic acid (DNBS)-, oxazolone-, and de

101 2,4-Dinitrobenzene sulfonic acid (DNBS)-induced colitis is a

102 Adoptive transfer of 2,4-dinitrobenzene sulfonic acid (DNBS)-pulsed DCs directly

103 gnificantly increased in colon tissues after dinitrobenzene sulfonic acid administration.

104 mononuclear cells (PBMCs)-DCs) treated with dinitrobenzene sulfonic acid for predicting skin-sensiti

105 of peripheral organ inflammation (i.e., 2,4-dinitrobenzene sulfonic acid-induced colitis).

106 is induced by intracolonic administration of dinitrobenzene sulfonic acid.

107 aced more effectively by the pi acceptor 2,4-dinitrobenzene than by the pi donor naphthalene.

108 lly if at all hypersensitive to 1-chloro-2,4-dinitrobenzene, the most commonly used substrate for glu

109 H(ab) values range from 5410 cm(-)(1) (1,4- dinitrobenzene) to 3400 cm(-)(1) (9,9-dimethyl-2,7-dinit

110 performed with a series of dinitrotoluenes, dinitrobenzene, trinitrotoluene, trinitrobenzene, two am

111 tal hepatic GST activity toward 1-chloro-2,4-dinitrobenzene was also significantly decreased.

112 1,5-difluoro-2,4-dinitrobenzene was conjugated at the C-terminal lysine f

113 Cross-linking the dimer by 1,5-difluoro-2,4-dinitrobenzene was inhibited by ATP, dATP, dGTP, and dAd