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1 ed glycolysis using either 2-deoxyglucose or iodoacetic acid.
2 g disulfide bonds and alkylation with [(13)C]iodoacetic acid.
3 Free sulfhydryl was first alkylated with 12C iodoacetic acid.
4 disulfide bonds, was then alkylated with 13C iodoacetic acid.
5 an the same peptide that was modified by 12C iodoacetic acid.
6 lar ATP levels, including cytochalasin B and iodoacetic acid.
7 of the cells in the presence of radiolabeled iodoacetic acid.
8 Chemical modification experiments with [14C]iodoacetic acid and 4-vinylpyridine determined that the
10 chlorosuccinimide, elastinal, iodoacetamide, iodoacetic acid, and phenylglyoxal gave substantial inhi
11 Glucosamine, 2-deoxyglucose, phloridzin, and iodoacetic acid blocked the activation of glucose-respon
12 llular Na+, or by glycolytic inhibition with iodoacetic acid blocked the subsequent effect of hydroge
17 ol based on the blocking of free thiols with iodoacetic acid, forming the carboxymethyl derivative of
19 erated oxidative stress with a rank order of iodoacetic acid (IAA) > bromoacetic acid (BAA) >> chloro
20 hylmaleimide (NEM), iodoacetamide (IAM), and iodoacetic acid (IAA) in alkylating protein thiols and f
25 , when the cells were treated with 75 microM iodoacetic acid (IAA), a metabolic inhibitor that induce
26 re usually reacted with iodoacetamide (IAM), iodoacetic acid (IAA), or another electrophile to preven
28 Kinase activity is relatively insensitive to iodoacetic acid (IAAcid) and iodoacetamide (IAAmide), th
30 netically in opsin(-/-) mice or acutely with iodoacetic acid) inhibited the expected diabetes-induced
31 n GSH-reduced PSP was carboxymethylated with iodoacetic acid, it still depended on extracellular GSH
34 s, either in the thiol form or modified with iodoacetic acid or methyl iodide, were grown into amyloi
36 lmethanesulfonyl fluoride, N-ethylmaleimide, iodoacetic acid, Pefabloc SC, and others) inhibited neit
37 iles dehydromonocrotaline, benzoquinone, and iodoacetic acid permitted their detection in a complex t
38 was fully (N-methylmaleimide) or partially (iodoacetic acid) reversed by DTT and inhibited by ruthen
39 ontaining peptides that were modified by 13C iodoacetic acid showed a molecular weight that was 2 Da
41 cation of the catalytic cysteine of PTP1B by iodoacetic acid, suggesting that it should be possible t
42 Inactivation of CHS by iodoacetamide and iodoacetic acid targets Cys(164) in a pH-dependent manne
45 ine hydrochloride and alkylation with [(12)C]iodoacetic acid, which was followed by reduction of the
47 ing reduction, differential alkylation using iodoacetic acid with either natural isotopes or enriched
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