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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.
16                  The electrochemistry of 1,2-dinitrobenzene (1,2-DNB), 1,3-dinitrobenzene (1,3-DNB),
17         Normalized response profiles for 1,3-dinitrobenzene (1,3-DNB) are independent of analyte conc
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
27              Cells treated with 1-chloro-2,4-dinitrobenzene, an irreversible inhibitor of thioredoxin
28  response is obtained for the explosives 1,3-dinitrobenzene and 2,4-dinitrotoluene over the 200-1,400
29 emically distinct sensitizers; 1-fluoro-2, 4-dinitrobenzene and 2-deoxyurushiol.
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
33 a12,14-prostaglandin-J2, menadione, 1-Cl-2,4-dinitrobenzene, and biotinylated iodoacetamide.
34 cal inhibitor of Trx reductase, 1-chloro-2,4-dinitrobenzene, and Trx1 siRNA.
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
38                           With 1-chloro-2, 4-dinitrobenzene as a substrate, the His107 residue primar
39 tt2p exhibit GST activity with 1-chloro-2, 4-dinitrobenzene as a substrate.
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
42          We demonstrate the utility of 4,5-o-dinitrobenzenes as relatively stable precursors to this
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
46         1,5-Bis-(dihexyl-N-nitrosoamino)-2,4-dinitrobenzene (C6') and an inactive form of the compoun
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
52      When the general substrate 1-chloro-2-4-dinitrobenzene (CDNB) was used to assess GST activity wi
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
55                                 1-Chloro-2,4-dinitrobenzene (CDNB), which causes oxidative stress thr
56  in the crystal between GSH and 1-chloro-2,4-dinitrobenzene (CDNB).
57  with respect to turnover with 1-chloro-2, 4-dinitrobenzene (CDNB).
58 GSH but not for the cosubstrate 1-chloro-2,4-dinitrobenzene (CDNB).
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
61                             The 1-fluoro-2,4-dinitrobenzene-conjugated dendritic cells that had been
62 P70 produced a reduction in the 1-fluoro-2,4-dinitrobenzene contact hypersensitivity response and res
63                    pi-pi EDA interactions of dinitrobenzene contribute -17 to -19 kJ/mol (3-3.4 log u
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
66                              Exposure to 1,3-dinitrobenzene (DNB) is associated with neuropathologic
67                          The location of the dinitrobenzene (DNB) ring in the GSDNB-GSTM2-2 complex w
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
71  respect to their response to the toxicant m-dinitrobenzene (DNB).
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
76          Chronic application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to
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
88 t release is rate-limiting when 1-chloro-2,4-dinitrobenzene is the substrate.
89                       In particular, the 1,3-dinitrobenzene isomer showed a higher proton transfer ra
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
92       The electron-withdrawing nature of the dinitrobenzene moieties can trigger the intramolecular H
93   Both mutants handle substrate 1-chloro-2,4-dinitrobenzene normally; however, Y103S exhibits a 30-fo
94 ein that is induced when the GST substrate o-dinitrobenzene (o-DNB) is added to the culture.
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
98 -transfer rates for the potassium salts of p-dinitrobenzene radical anion (DNB(-)).
99 ar unsymmetrical gas-phase structure for 1,3-dinitrobenzene radical anion but give serious spin conta
100 romyces cerevisiae leads to an increase in o-dinitrobenzene resistance in S. cerevisiae cells.
101 thione (GSH), by treatment with 1-chloro-2,4-dinitrobenzene, resulted in increased dense cells.
102 control, L19K was conjugated to 1-fluoro-2,4-dinitrobenzene, resulting in L19K-DNP.
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
111                                          2,4-Dinitrobenzene sulfonic acid (DNBS)-induced colitis is a
112                     Adoptive transfer of 2,4-dinitrobenzene sulfonic acid (DNBS)-pulsed DCs directly
113 gnificantly increased in colon tissues after dinitrobenzene sulfonic acid administration.
114  mononuclear cells (PBMCs)-DCs) treated with dinitrobenzene sulfonic acid for predicting skin-sensiti
115  of peripheral organ inflammation (i.e., 2,4-dinitrobenzene sulfonic acid-induced colitis).
116 is induced by intracolonic administration of dinitrobenzene sulfonic acid.
117 aced more effectively by the pi acceptor 2,4-dinitrobenzene than by the pi donor naphthalene.
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
121 tal hepatic GST activity toward 1-chloro-2,4-dinitrobenzene was also significantly decreased.
122                             1,5-difluoro-2,4-dinitrobenzene was conjugated at the C-terminal lysine f
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

 
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