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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
10 luoromethoxy-phenylhydrazone (1-3 nM) or 2,4-dinitrophenol (100 nM) significantly antagonized and del
11 hibitors noeuromycin, mannoimidazole, or 2,4-dinitrophenol 2-deoxy-2-fluoro-mannoside reveal the resi
12 the genes involved in the degradation of 2,4-dinitrophenol (2,4-DNP) in a Rhodococcus erythropolis st
14 the inhibitors, conduritol beta-epoxide and dinitrophenol-2-deoxy-2-fluoro-beta-D-glucopyranoside (D
15 environment on the rate of photolysis of 2,4-dinitrophenol (24-DNP), an important environmental toxin
16 photolysis of 4-nitrocatechol (4NC) and 2,4-dinitrophenol (24DNP) in semisolid isomalt as a new type
17 yanide m-chlorophenylhydrazone, 44%, and 2,4-dinitrophenol, 26%), by sodium azide (25%), and hydroxyl
19 on of HTC hepatoma cells by exposure to 2, 4-dinitrophenol (50 microM) and 2-deoxy-D-glucose (10 mM)
22 e (AICAR), rotenone (a Complex I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contra
24 COUPY-caged version of the protonophore 2,4-dinitrophenol allowed us to confirm by confocal microsco
25 loped method can be used to detect trace 2,4-dinitrophenol, an explosive, with a limit of detection a
27 somes is ATP-dependent, and ATP depletion by dinitrophenol and 2-deoxyglucose also inhibited apoB deg
28 s potent than the prototypical uncoupler 2,4-dinitrophenol and phenocopies 2,4-dinitrophenol in lower
29 io calculations which show that 2,3- and 2,6-dinitrophenol and picric acid are significantly distorte
30 o resolve time-depending binding between 2,4-dinitrophenol and transthyretin, and analyze biologicall
32 lex 1 inhibitor (rotenone) and an uncoupler (dinitrophenol) and by overexpression of mGPDH, which low
33 nic acid), electrophilic substrate analogue (dinitrophenol), and product analogues (S-hexylglutathion
34 ropic agent chloroquine, the energy depleter dinitrophenol, and also by low temperature, suggesting t
35 m: carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5 killing of Cand
36 Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5-induced ATP eff
37 cell lines or colonic biopsy specimens using dinitrophenol, and barrier function was assessed by tran
38 ated that sodium salicylate, plumbagin, 2, 4-dinitrophenol, and menadione-inducers of the marRAB oper
39 arbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophenol, and nigericin but not by the potassium io
40 -hydroxy-2-nonenal (HNE) -modified proteins, dinitrophenol, and nitrotyrosine to quantify and localiz
41 amino acid secretions was verified using 2,4-dinitrophenol as an inhibitor of the proton motive force
42 2-aminobenzyl-GGFLRKVGQ-ethylenediamine-2,4-dinitrophenol at the R-K bond, exhibiting a K(m) of 13 m
44 ress and the mitochondrial uncoupling agent, dinitrophenol, both of which lead to increased glucose t
46 ol C6H5NO4, methylnitrocatechol C7H7NO4, and dinitrophenol C6H4N2O5) measured with a micro-orifice vo
47 of these cells by macrophages; and (3) that dinitrophenol can be used as a surrogate for quantitatin
48 bind putative ligands of the EmrAB pump-2,4-dinitrophenol, carbonyl cyanide m-chlorophenylhydrazone,
49 ing of a haptenated fluorescent protein, 2,4-dinitrophenol-coupled B-phycoerythrin (DNP25-PE), to flu
51 I(H) is induced by protonophores such as 2,4-dinitrophenol (DNP) and cyanide-4-(trifluoromethoxy) phe
54 n be quenched by both the negatively charged dinitrophenol (DNP) derivative, (DNP-BS(-)), and positiv
56 on of the mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) in a large animal model with minimum
57 efficacy of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) in animals receiving striatal inject
60 vical spinal cord transection, NaCN and also dinitrophenol (DNP) significantly (P < 0.05) elevated rC
61 od are demonstrated using the binding of 2,4-dinitrophenol (DNP) to transthyretin (TTR), as well as p
63 the presence of the mitochondrial uncoupler dinitrophenol (DNP) were compared using 16.4 T in isoflu
64 itro explosives, i.e., picric acid (PA), 2,4-dinitrophenol (DNP), and nitrophenol (NP), via the fluor
65 III, or by the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), indicating ATP depletion causes the
66 onyl cyanide m-chlorophenylhydrazone (CCCP), dinitrophenol (DNP), or CN(-), resulted in massive disso
67 of increased UCP3 expression), and acute 2,4-dinitrophenol (DNP)-treated (protonophore and mitochondr
70 ole-cell recordings, bath application of 2,4-dinitrophenol (DNP, an uncoupler of mitochondrial ATP pr
71 CsA, 42.6+/-9.0% with SfA; P<0.001), or 2,4-dinitrophenol (DNP, the mitochondrial uncoupler, 50 micr
72 acetate (IAA; glycolysis inhibitor) plus 2,4-dinitrophenol (DNP; oxidative phosphorylation inhibitor)
73 surface-bound IgG molecules (on various 2,4-dinitrophenol [DNP]-coated surfaces and pathogenic Staph
75 -N-oxide and 2-[1-(p-chlorophenyl)ethyl] 4,6-dinitrophenol establish that both inhibitors block the b
76 e heat shock response, including salicylate, dinitrophenol, ethanol, and arsenite, have no effect on
78 PH), a primary antibody specific for the 2,4-dinitrophenol group, and a peroxidase-labeled second ant
80 ans blue dye in mice passively sensitized to dinitrophenol-human serum albumin and challenged intrade
81 so studied in mice passively sensitized with dinitrophenol-human serum albumin and challenged intrade
83 oupler 2,4-dinitrophenol and phenocopies 2,4-dinitrophenol in lowering de novo lipogenesis and mitoch
84 ophilic analog of the uncoupler compound 2,6-dinitrophenol, in which a C8-hydrocarbon chain was conju
86 We have previously reported that 2-alkyl-4,6-dinitrophenols inhibit mammalian complexes I, II, and II
87 ide-4-(trifluoromethoxy) phenylhydrazone and dinitrophenol inhibited inositol transport by 50-70% in
88 nide-4-(trifluoromethoxy)phenylhydrazone and dinitrophenol inhibited inositol transport by 50-70% in
90 stearoyl-oleoyl-phosphatidylcholine plus 3% dinitrophenol-linked di-oleoyl-phosphatidylethanolamine.
91 lic cation and releases the protonophore 2,4-dinitrophenol locally in predetermined regions in respon
93 e protective effect of pretreatment with 2,4-dinitrophenol, measured from increased functional recove
95 tion by 150 microM GS-Succ-BP is provided by dinitrophenol, nitrobenzene, ethacrynic acid, and S-hexy
96 er, serious adverse effects of the uncoupler dinitrophenol occurred when used to increase significant
98 Out of six possible positional isomers of dinitrophenol, only 2,4-DNP has been used extensively by
99 inhibitors of ATP synthesis (oligomycin, 2,4-dinitrophenol, or 2-deoxyglucose) made them more suscept
102 Addition of the metabolic poisons cyanide or dinitrophenol reduced the active transport of both prote
104 pleted by treatment with sodium azide or 2,4-dinitrophenol; restoration of the original ATP levels oc
107 mitochondrial membrane potential uncoupler, dinitrophenol, supporting a role for mitochondrial regul
108 l assays for the environmental pollutant 2,4-dinitrophenol the alternative devices were 50% more sens
109 rs with very good leaving groups such as 2,4-dinitrophenol, the monoanion of phosphate esters is more
110 Treatment of the FF group with low dose 2,4-dinitrophenol to increase energy expenditure abrogated t
111 fect of four environmental contaminants, 2,4-dinitrophenol, triclosan, n-(1,3-dimethylbutyl)-N'-pheny
113 ies we have selected a series of 2-alkyl-4,6-dinitrophenols which proved to be very effective noncomp
115 y reduced binding to both salicylate and 2,4-dinitrophenol, while a mutation in residue H19 impaired