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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
9 the stable isotopic labeling reagents [12C2]-iodoacetic acid and [13C2]-bromoacetic acid.
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
13            Recombinant Trx1 was sensitive to iodoacetic acid but showed strong resistance to oxidatio
14         Moreover, neither mutant reacts with iodoacetic acid, demonstrating selectivity of the largel
15                                The amount of iodoacetic acid-derived radioactivity associated with PT
16          In contrast, alkylation of Cys with iodoacetic acid did not prevent Zn2+ binding to the HMA2
17 ol based on the blocking of free thiols with iodoacetic acid, forming the carboxymethyl derivative of
18 by reaction of dithiothreitol with tritiated iodoacetic acid (I-C[3H(2)].CO(2)H).
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
21                Here, the authors evaluate an iodoacetic acid (IAA) model of photoreceptor degeneratio
22 ficant inactivation was observed with either iodoacetic acid (IAA) or bromoacetic acid (BAA).
23                                  Addition of iodoacetic acid (IAA) resulted in diversion of purine ra
24 protect HT-22 cells from either glutamate or iodoacetic acid (IAA) toxicity.
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
27 ction of disulfide bonds and alkylation with iodoacetic acid (IAA).
28 Kinase activity is relatively insensitive to iodoacetic acid (IAAcid) and iodoacetamide (IAAmide), th
29                                              Iodoacetic acid inhibited wild-type enzyme activity in a
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
32                 Reaction of this mutant with iodoacetic acid led to approximately one less mole of re
33     The percentage of modification by [(12)C]iodoacetic acid of each cysteine residue was calculated
34 s, either in the thiol form or modified with iodoacetic acid or methyl iodide, were grown into amyloi
35 P31 required the addition of dithiothreitol, iodoacetic acid, or N-ethylmaleimide.
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
40                                Inhibition by iodoacetic acid suggested that both the expressed enzyme
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
43 n vivo by genetic (opsin(-/-)) and chemical (iodoacetic acid) techniques.
44                                              Iodoacetic acid toxicity was mitigated by antioxidants,
45 ine hydrochloride and alkylation with [(12)C]iodoacetic acid, which was followed by reduction of the
46 ng peptide, corresponding to modification by iodoacetic acid with 12C or 13C.
47 ing reduction, differential alkylation using iodoacetic acid with either natural isotopes or enriched

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