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1 covered and designated ROD1 (resistance to o-dinitrobenzene).
2 -1 for the native enzyme toward 1-chloro-2,4-dinitrobenzene.
3 e experimental contact allergen 1-fluoro-2,4-dinitrobenzene.
4 nzyme's preferred substrate is 1-chloro-2, 4-dinitrobenzene.
5 glutathione sulfonic acid, and glutathione-s-dinitrobenzene.
6 to discriminate between the three isomers of dinitrobenzene.
7 esized bearing 1 to 4 sulfonamide-linked 2,4-dinitrobenzene.
8 ,3,5-trinitro-1,3,5-triazinane, and DNB: 1,3-dinitrobenzene.
9 ding unique responses for dinitrotoluene and dinitrobenzene.
10 ect transferase activity toward 1-chloro-2,4-dinitrobenzene.
11 xed saturating concentration of 1-chloro-2,4-dinitrobenzene.
12 rom that of monobromobimane and 1-chloro-2,4 dinitrobenzene.
13 elated to substrates, including 1-chloro-2,4-dinitrobenzene.
14 ted by the GSH-specific reagent 1-chloro-2,4-dinitrobenzene.
15 d reductive cyclization of 1,4-dialkenyl-2,3-dinitrobenzenes.
18 emistry of 1,2-dinitrobenzene (1,2-DNB), 1,3-dinitrobenzene (1,3-DNB), and 1,4-dinitrobenzene (1,4-DN
19 -DNB), 1,3-dinitrobenzene (1,3-DNB), and 1,4-dinitrobenzene (1,4-DNB) is strongly affected by the pre
20 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
21 xide diamine (HMTD), 2,4-dinitrotoluene, 1,3-dinitrobenzene, 1,3,5-trinitrobenzene, 2-amino-4,6-dinit
22 dinitroaromatic radical anions (1,2- and 1,4-dinitrobenzene, 1,5- and 2,6-dinitro naphthalene, 4,4'-d
23 ocalized) intervalence radical anions of 1,4-dinitrobenzene, 2,6-dinitronaphthalene, 2,6-dinitroanthr
24 inity peptide tag, (64)Cu-L19K-(5-fluoro-2,4-dinitrobenzene) ((64)Cu-L19K-FDNB), which binds covalent
25 ddition of glutathione (GSH) to 1-chloro-2,4-dinitrobenzene, a reaction in which the chemical step is
26 eater than marginal activity with chloro-2,4 dinitrobenzene activity also exhibited significant activ
28 response is obtained for the explosives 1,3-dinitrobenzene and 2,4-dinitrotoluene over the 200-1,400
30 th 92% residual activity toward 1-chloro-2,4-dinitrobenzene and completely blocks Cys111 from subsequ
31 appreciable changes in K(m) for 1-chloro-2,4-dinitrobenzene and have similar CD spectra to that of wi
32 omatic compounds (1,3,5 trinitrobenzene, 1,3 dinitrobenzene, and 2,4 dinitrotoluene) and electronic s
35 ith CuCN x 2LiBr and then oxidizing with 1,3-dinitrobenzene, and was used in a diversity-oriented syn
36 25 M(-1) s(-1)) compared to that of the 1,2-dinitrobenzene ( approximately 5 M(-1) s(-1)), whereas t
37 ic substrate sites (such as for 1-chloro-2,4-dinitrobenzene) are predominantly located within each su
40 nits/mg of cytosolic protein, using 1-Cl-2,4-dinitrobenzene as substrate), resulted in 70-90% reducti
41 tivities toward dimethenamid or 1-chloro-2,4-dinitrobenzene as substrates and in their levels of indu
43 enzyme was highly active toward 1-chloro-2,4-dinitrobenzene, as well as chloroacetanilide herbicides.
44 uctase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H(2)O(2) removal rates in mit
45 ncrease in GST activity toward 1-chloro-2, 4-dinitrobenzene but GST activity toward 4-HNE was increas
47 of the compound [1,5-bis-(dihexylamino)-2,4-dinitrobenzene (C6)] were tested in neuronal cell cultur
48 ls of enzymatic activity toward 1-chloro-2,4-dinitrobenzene (CDNB) and HNE were present in normal ste
49 is based on competition between 1-chloro-2,4-dinitrobenzene (CDNB) and the drugs for the GST enzyme i
50 exhibited high activity with 1-chloro-2, 4, dinitrobenzene (CDNB) but low activity with the chloroac
51 eaction between glutathione and 1-chloro-2,4-dinitrobenzene (CDNB) is widely used as a standard activ
53 ly) the canonical GST substrate 1-chloro-2,4-dinitrobenzene (CDNB), and bear a wide variety of bioort
54 mmonly used synthetic substrate 1-chloro-2,4-dinitrobenzene (CDNB), but has relatively high glutathio
59 hionine S,R-sulfoximine (BSO); 1-chloro, 2,4-dinitrobenzene (CDNB); or 1,3-bis (2-chloroethyl)-1-nitr
60 porter gene to screen a 1,5-dialkylamino-2,4-dinitrobenzene combinatorial chemical library consisting
62 P70 produced a reduction in the 1-fluoro-2,4-dinitrobenzene contact hypersensitivity response and res
64 droxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2
65 pproximately 5 M(-1) s(-1)), whereas the 1,4-dinitrobenzene did not show any proton transfer effect i
68 rinitrobenzene (TNB), trinitrotoluene (TNT), dinitrobenzene (DNB), tetryl, and 2,4-dinitrotoluene (2,
69 he redox potentials of compounds such as 1,4-dinitrobenzene (DNB), which can be reduced in two one-el
70 roteins as a function of sensitivity to 1, 3-dinitrobenzene (DNB)-induced mitochondrial permeability
72 carboxylic acid electron acceptors including dinitrobenzenes (DNBs) and naphthalenediimide (NI), whic
73 report that a contact allergen, 1-chloro-2,4-dinitrobenzene (DNCB), elicits contact hypersensitivity
74 or the Trx reductase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB), in embryonic rat heart (H9c2) cel
75 ation with the contact allergen 1-fluoro-2,4-dinitrobenzene (DNFB) resulted in epidermal accumulation
77 AN9 toward the common substrate 1-chloro 2,4-dinitrobenzene, equilibrium dialysis, and tryptophan que
78 s more than 50-fold greater for 1-fluoro-2,4-dinitrobenzene (FDNB), and the product is the same for b
79 trate-dependent; in contrast to 1-chloro-2,4-dinitrobenzene, for the nucleophilic addition reaction o
80 nated peptide ions and radical anions of 1,3-dinitrobenzene formed exclusively c- and z-type fragment
81 ed sorption of benzene, naphthalene, and 1,4-dinitrobenzene from water to a series of wood chars made
82 hGSTM1a-1a complexed with 1-glutathionyl-2,4-dinitrobenzene (GS-DNB) formed by a reaction in the crys
83 nto DTY167 cells alleviates the 1-chloro-2,4-dinitrobenzene-hypersensitive phenotype concomitant with
84 active site alters affinity for 1-chloro-2,4-dinitrobenzene in the active site of the other subunit.
85 red forms by potassium-mirror reduction of p-dinitrobenzene in the presence of macrocyclic polyether
86 catalyze conjugation of GSH to 1-chloro-2,4-dinitrobenzene, indicating an absence of microsomal glut
87 tely inhibited activity toward 1-chloro-2, 4-dinitrobenzene, indicating that AFB-GSH binding to one a
90 d of electrogenerated dianionic species from dinitrobenzene isomers and substituted dihomooxacalix[4]
91 the complete discrimination of very similar dinitrobenzene isomers and three halogenated, substitute
93 Both mutants handle substrate 1-chloro-2,4-dinitrobenzene normally; however, Y103S exhibits a 30-fo
95 plosives-related compounds nitrobenzene, 1,3-dinitrobenzene, o-nitrotoluene, 2,4-dinitrotoluene, and
96 vity (induced by treatment with 1-chloro-2,4-dinitrobenzene) or brush stimulation-induced AD-like ski
97 oluene, 2,6-dinitrotoluene, trinitrobenzene, dinitrobenzene, or 1,3,5-trinitro-1,3,5-triazacyclohexan
99 ar unsymmetrical gas-phase structure for 1,3-dinitrobenzene radical anion but give serious spin conta
103 dynein and myosin V using 1,5-difluoro-2, 4-dinitrobenzene revealed that this light chain exists as
104 n as that of the enzyme-GSH complex, and the dinitrobenzene ring is anchored between the side chains
105 minobenzoic acid substituent is bound to the dinitrobenzene ring via its carboxyl oxygen while the ot
106 diaminobenzoquinone diimine units linked by dinitrobenzene rings, are synthesized by selective oxida
107 On percutaneous immunization to 1-fluoro-2,4-dinitrobenzene, stimulated CD4(+) T cells from draining
108 nin-specific TH1 clone) or with 5S8 T cells (dinitrobenzene sulfonate specific Th0 clone) in the pres
109 induced with dextran sulfate sodium (DSS) or dinitrobenzene sulfonic acid (DNBS) in mice treated with
110 e mice significantly reduced the severity of dinitrobenzene sulfonic acid (DNBS)-, oxazolone-, and de
114 mononuclear cells (PBMCs)-DCs) treated with dinitrobenzene sulfonic acid for predicting skin-sensiti
118 lly if at all hypersensitive to 1-chloro-2,4-dinitrobenzene, the most commonly used substrate for glu
119 H(ab) values range from 5410 cm(-)(1) (1,4- dinitrobenzene) to 3400 cm(-)(1) (9,9-dimethyl-2,7-dinit
120 performed with a series of dinitrotoluenes, dinitrobenzene, trinitrotoluene, trinitrobenzene, two am
123 Cross-linking the dimer by 1,5-difluoro-2,4-dinitrobenzene was inhibited by ATP, dATP, dGTP, and dAd
124 ita-Stille cross coupling of 1,4-dibromo-2,3-dinitrobenzene with an alkenyltin reagent to give symmet