ライフサイエンスコーパス: iodoacetate

1 (MTSES(-), MTSET(+), MMTS(0), MTSHE(0), and iodoacetate(-)).

2 olic insult (5 mM potassium cyanide and 1 mM iodoacetate).

3 of cells after inhibition of glycolysis with iodoacetate.

4 ylation of the cob(I)alamin nucleophile with iodoacetate.

5 ferent stages by alkylating free thiols with iodoacetate.

6 AIA were similar to their reactivities with iodoacetate.

7 potential regulatory site-directed reagents: iodoacetate, 1,3-dibromoacetone, and 1-bromo-2-butanone.

8 chemical inhibitors of phagocytosis such as iodoacetate, 2-deoxyglucose, gadolinium chloride, and cy

9 of cyanide or rotenone, 2) are suppressed by iodoacetate, 3) are accompanied by at most very small mi

10 te that impairment of glucose metabolism via iodoacetate, a glyceraldehyde-3-phosphate dehydrogenase

11 The site of pyruvate and iodoacetate action was shown to be a different sulfhydry

12 ors phenylarsine oxide, sodium vanadate, and iodoacetate also inhibited enzyme activity.

13 Furthermore, uH2B induction is inhibited by iodoacetate, an inhibitor of glyceraldehyde-3-phosphate

14 foetus was inactivated by the thiol reagents iodoacetate and 5,5'-dithiobis(2-nitrobenzoic acid) (Nbs

15 The metabolic inhibitors iodoacetate and 6-aminonicotinamide at concentrations wh

16 protection against HGXPRTase inactivation by iodoacetate and against carboxymethylation of Cys129, Cy

17 symmetric Reformatsky reaction between ethyl iodoacetate and aldehydes.

18 quence and amino acid analysis revealed that iodoacetate and ClAc-DMDDF had reacted with both active

19 glucose deprivation or glycolytic inhibitors iodoacetate and sodium fluoride synergistically cooperat

20 astereoselective radical cascade using ethyl iodoacetate and triethylborane is described.

21 Like PTPs, this enzyme was inhibited by iodoacetate and VO43- and independent of Mg2+, providing

22 ery low level when glycolysis was blocked by iodoacetate, and inclusion of lactate, pyruvate, glutama

23 Using iodoacetate as the warhead, 8-base PNA strands, biotin,

24 Iodoacetate at 10 mM reduced the Hill coefficient from 2

25 The presence of pyruvate or iodoacetate blocked inhibition of the enzyme by N-ethylm

26 ox-active regulatory disulfide bond, because iodoacetate bound to the alternative oxidase at the acti

27 tion that Ca2+ transients were suppressed by iodoacetate but unaffected by mitochondrial inhibitors.

28 as not protected by either substrate against iodoacetate, but its carboxymethylation caused no loss i

29 ecretion was inhibited by 2-deoxyglucose and iodoacetate, confirming active secretion.

30 Inactivation of both wt and T298C by iodoacetate elicits a pseudo-first-order loss of activit

31 Inhibiting glycolysis with iodoacetate eliminated the protective effects of FBP in

32 Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and

33 Pretreatment of the enzyme with iodoacetate has no effect on signal formation with ferri

34 tochondrial respiratory chain inhibitor) and iodoacetate [IA, an inhibitor of the glycolytic enzyme g

35 cts of inhibitors (2-deoxy-D-glucose (2-DG), iodoacetate (IAA)), intermediates (glucose-6-phosphate (

36 f the cells with an inhibitor of glycolysis, iodoacetate (IAA; 0.5 mm), did not prevent the effects o

37 oavailability in rat and efficacy in the rat iodoacetate in vivo model.

38 Inhibiting glycolysis by 2-deoxyglucose or iodoacetate, in the presence of glucose, reversed the pr

39 Iodoacetate inactivates the enzyme in a time-dependent a

40 tion experiments with a substrate (pNPP) and iodoacetate indicate that TBNS is active site-directed.

41 of iodine and yet were poorly modified with iodoacetate led us to suggest that the pairs of residues

42 enerated by intraarticular injection of mono-iodoacetate (MIA) in Sprague-Dawley rats, and symptomati

43 on by intraarticular injection of monosodium iodoacetate (MIA) into facet joints (L3-L4, L4-L5, L5-L6

44 s by intraarticular injection of sodium mono-iodoacetate (MIA), and the development of pain behavior

45 During metabolic inhibition (CN and iodoacetate) of isolated myocytes stimulated at 1 Hz, th

46 as glycolytic inhibitors (2-deoxyglucose and iodoacetate) on the induction and maintenance of apoptos

47 ce, or following inhibition of glycolysis by iodoacetate or 2-deoxyglucose.

48 rolysis of the protein alkylated with either iodoacetate or 3-bromopropionate yielded Se-carboxymethy

49 glycolytic flux by application of pyruvate, iodoacetate or beta-hydroxybutyrate induced electromecha

50 itochondria were isolated in the presence of iodoacetate or N-ethylmaleimide, the intermolecular disu

51 on of cysteine residues 129, 132, and 148 by iodoacetate or Nbs2 hinders substrate binding which can,

52 or 3-nitropropionic acid) or of glycolysis (iodoacetate plus pyruvate) also produced only partial AT

53 Moreover, blastocysts treated with iodoacetate result in poor pregnancy outcome as determin

54 tive site cysteine with the alkylating agent iodoacetate results in a loss of binding affinity.

55 The GAPDH inhibitor iodoacetate suppressed GAPDH/3-PGK-dependent, but not ex

56 Tocopherol iodoacetate (TIA), a reactive analogue, produces a time-

57 Iodoacetate-trapped I-1 and I-2 contain low alpha-helica

58 experiments indicate that reduced rhSCF and iodoacetate-trapped I-1, I-2, and I-3 exist as dimeric f

59 inhibited alternative oxidase activity, but iodoacetate was found to stimulate activity much like py

60 the observation that total inactivation with iodoacetate was not achieved suggests that none of the r

61 cetamido) fluorescein, IAEDANS, pyrenemethyl iodoacetate) were attached to these residues.

62 e of metabolic substrates and was blocked by iodoacetate, which is an inhibitor of glycolysis.

63 he covalent adduct formed by the reaction of iodoacetate with sulfhydryls, the activation of the alte