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1 atment with the histidine-modifying compound diethylpyrocarbonate.
2 tive to N-ethylmaleimide, phenylglyoxal, and diethylpyrocarbonate.
3 activated by the histidine-modifying reagent diethylpyrocarbonate.
4 with RNases T1 and V1 and the small molecule diethylpyrocarbonate.
5 form, and hypochlorite but more resistant to diethylpyrocarbonate.
6 different covalent labeling reagents, namely diethylpyrocarbonate, 2,3-butanedione, and the reagent p
7 is finding contradicts earlier results using diethylpyrocarbonate alone, which suggested an RNA synth
8 r clearance by using potassium permanganate, diethylpyrocarbonate and methidiumpropylEDTA.Fe(II) foot
9      The enzyme exhibited sensitivity toward diethylpyrocarbonate and some thiol-directed reagents, a
10 oscopy, histidine modification studies using diethylpyrocarbonate, and enzymatic activity measurement
11  to N-ethylmaleimide, F-, phenylglyoxal, and diethylpyrocarbonate, both substrates appear to be hydro
12 it was shown that both histidines react with diethylpyrocarbonate but that only reaction with His-8 r
13  by quinine, Gd3+, La3+ and the His modifier diethylpyrocarbonate, but not by the Ca2+ or K+ channel
14 me A (OSB-CoA) synthetase, when treated with diethylpyrocarbonate (DEP), showed a time-dependent loss
15 studies involving chemical modification with diethylpyrocarbonate (DEPC) and site-directed mutagenesi
16 ut protein-ligand binding when reagents like diethylpyrocarbonate (DEPC) are used for CL because of t
17   The reliability and information content of diethylpyrocarbonate (DEPC) as a covalent probe of prote
18 ication of histidyl residues of tubulin with diethylpyrocarbonate (DEPC) at a mole ratio of 0.74 (DEP
19           In this study, we demonstrate that diethylpyrocarbonate (DEPC) covalent labeling mass spect
20                In this study, we investigate diethylpyrocarbonate (DEPC) covalent labeling-mass spect
21                In this study, we investigate diethylpyrocarbonate (DEPC) covalent labeling-mass spect
22 yme, H61A, H62A, and H79A, and the effect of diethylpyrocarbonate (DEPC) have been investigated to el
23                                              Diethylpyrocarbonate (DEPC) is a simple to use, commerci
24                                              Diethylpyrocarbonate (DEPC) labeling analyzed with mass
25 g sites at the N protein were identified via diethylpyrocarbonate (DEPC) labeling and bottom-up prote
26 In this work, we describe a method that uses diethylpyrocarbonate (DEPC) labeling and mass spectromet
27    Experiments with the His-specific reagent diethylpyrocarbonate (DEPC) showed that one or more His
28                                              Diethylpyrocarbonate (DEPC) treatment of the protein abo
29            The chemical modification reagent diethylpyrocarbonate (DEPC) was used to modify alpha 1-a
30 , alpha,beta-unsaturated carbonyl (ABUC) and diethylpyrocarbonate (DEPC), and insulin and beta2-micro
31 ibitory binding site was also assessed using diethylpyrocarbonate (DEPC), which modifies histidines.
32                         In this work, we use diethylpyrocarbonate (DEPC)-based covalent labeling toge
33 MOB (H5 and H33) were chemically modified by diethylpyrocarbonate (DEPC).
34 f the reversible histidine-modifying reagent diethylpyrocarbonate (DEPC).
35 natostilbene-2,2'-disulfonic acid (DIDS), or diethylpyrocarbonate (DEPC).
36 nate (CMCT; to probe U at N-3 and G at N-1), diethylpyrocarbonate (DEPC; to probe A at N-7), dimethyl
37                                              Diethylpyrocarbonate inactivated the enzyme in a reactio
38 estored 95% activity, results that indicated diethylpyrocarbonate inactivates the enzyme by the speci
39 thanosarcina thermophila was investigated by diethylpyrocarbonate inactivation and site-directed muta
40                                              Diethylpyrocarbonate inactivation of the eight histidine
41                                              Diethylpyrocarbonate pretreatment increased water permea
42 e modification reagents N-ethylmaleimide and diethylpyrocarbonate, respectively.
43        Inactivation of ACL by treatment with diethylpyrocarbonate suggested the catalytic role of an
44 ase reaction was suggested by the ability of diethylpyrocarbonate to block formation of mevalonate fr
45 ivity of zinc potentiation of alpha4beta4 to diethylpyrocarbonate treatment and alterations in pH sug
46 H:FR activities in a reversible manner while diethylpyrocarbonate treatment resulted in complete irre
47 to inhibit alpha4beta4 and alpha3beta2 after diethylpyrocarbonate treatment.
48 nated with ribonuclease unless the inhibitor diethylpyrocarbonate was used during the ribonucleic aci
49 kinetics of inactivation of E. coli Lgt with diethylpyrocarbonate were consistent with the modificati