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1 80% acetone or 100% acetone containing 0.1% diethyl pyrocarbonate.
2 so blocked by the histidine-reactive reagent diethyl pyrocarbonate.
3 ions inactivate LpxE, as does treatment with diethyl pyrocarbonate.
4 vity to osmium tetroxide, hydroxylamine, and diethyl pyrocarbonate.
5 by the histidine-selective acylating reagent diethyl pyrocarbonate.
6 ily reacting with the group specific reagent diethyl pyrocarbonate.
7 sidual activity was relatively unaffected by diethyl pyrocarbonate.
8 d mutagenesis and chemical modification with diethyl pyrocarbonate.
9 1 channel with the histidine modifying agent diethyl pyrocarbonate also enhanced the hSlo1 currents a
10 the internal pH sensitivity, suggesting that diethyl pyrocarbonate and low pH may work on the same ef
11 y due to inhibitory effects to the enzyme by diethyl pyrocarbonate and N-ethylmaleimide, respectively
12 lity of histidyl residues to modification by diethyl pyrocarbonate and observed that more than 50% pr
14 etal ions, and buffer conditions using OsO4, diethyl pyrocarbonate, and chloroacetaldehyde probes.
15 e was extremely susceptible to inhibition by diethyl pyrocarbonate, and protection against inhibition
16 ss spectrometry of the peptide modified with diethyl pyrocarbonate before and after Cu binding sugges
18 were no longer sensitive to inactivation by diethyl pyrocarbonate, demonstrating that this is the in
19 Each of the five mutants is inactivated by diethyl pyrocarbonate (DEP), and inactivation is reversi
21 ment with the reversible histidine-modifying diethyl pyrocarbonate (DEPC) inhibited acyltransferase a
25 thermophilus Rieske protein was reacted with diethyl pyrocarbonate (DEPC) over a range of pH values.
27 s more pronounced with hydrophobic reagents [diethyl pyrocarbonate (DEPC), p-bromophenacyl bromide] a
30 e presence of reversible histidine-modifying diethyl pyrocarbonate (DEPC); 0.3 mM DEPC results in 95%
31 utaryl-CoA (HMG-CoA) lyase is inactivated by diethyl pyrocarbonate (DEPC); activity can be fully rest
34 on of HGPRT with either tetranitromethane or diethyl pyrocarbonate inactivated the enzyme completely,
38 of EDTA or upon treatment of the enzyme with diethyl pyrocarbonate, it is proposed that Cu(2+) of L2
43 etioplasts with 100% acetone containing 0.1% diethyl pyrocarbonate prevents the conversion of Pchlide
44 istidine-selective inactivation studies with diethyl pyrocarbonate provide further evidence regarding
45 inines and histidines with phenylglyoxal and diethyl pyrocarbonate, respectively, renders the enzyme
49 ous biochemical investigations showed that a diethyl pyrocarbonate-sensitive histidine residue is at
51 Inhibition is observed in the presence of diethyl pyrocarbonate, suggesting that a histidine is cr
52 n the protection of His from modification by diethyl pyrocarbonate when this residue binds Cu(II) in
53 that Lit was susceptible to inactivation by diethyl pyrocarbonate, with about three histidines rever
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