ライフサイエンスコーパス: hyperoxidation

1 g to the protection of peroxiredoxin IV from hyperoxidation.

2 DJ-1 shows potentiated H2O2-induced Cys-106 hyperoxidation.

3 er, making it is more resistant than Prx2 to hyperoxidation.

4 onding Prx2 chimera became more resistant to hyperoxidation.

5 Prxs vary in susceptibility to hyperoxidation.

6 tive to inactivation by peroxide-induced Prx hyperoxidation.

7 l signaling and protects protein thiols from hyperoxidation.

8 ukaryotic peroxiredoxins by their reversible hyperoxidation.

9 t does not change the apparent mitochondrial hyperoxidation after anoxia.

10 the DJ-1 C106A mutant, which fully prevents hyperoxidation, also showed exacerbated cell death respo

11 Their activity can be regulated by hyperoxidation and consequent inactivation of the active

12 2-like protein with increased sensitivity to hyperoxidation and decreased ability to form the intermo

13 ength of anoxic depolarization can influence hyperoxidation and electrical activity recovery followin

14 icals in promoting post-anoxic mitochondrial hyperoxidation and electrical failure, and suggest that

15 er antioxidants could suppress mitochondrial hyperoxidation and improve electrical recovery after ano

16 formation as a protection mechanism against hyperoxidation and inactivation.

17 We report here that mitochondrial hyperoxidation and synaptic activity in hippocampal slic

18 to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism.

19 der adults exhibited higher levels of PRX1-3 hyperoxidation basally and under conditions of oxidative

20 dition, Prx2 was more sensitive than Prx1 to hyperoxidation caused by both urate hydroperoxide and hy

21 plasmic reticulum-localized peroxiredoxin to hyperoxidation compared with either the cytosolic or mit

22 r processes that involve redox cycling, with hyperoxidation controlling structural transitions that a

23 d rate constants for disulfide formation and hyperoxidation for human recombinant Prx2 and Prx3 by an

24 Our findings suggest that the hyperoxidation generated by Ero1alpha-C104A/C131A is add

25 of eukaryotic 2-Cys peroxiredoxins (Prxs) by hyperoxidation has been proposed to promote accumulation

26 rx1) exhibited both decreased expression and hyperoxidation in response to mutant Htt expressed in ei

27 Each enzyme is equally sensitive to hyperoxidation in the presence of a robust recycling sys

28 expression of Prdx4 is highly susceptible to hyperoxidation in the presence of high glucose.

29 Hyperoxidation inactivates the Prx and is implicated in

30 d NADPH) was necessary, indicating that such hyperoxidation occurs only when Prx I is engaged in the

31 This gave a second order rate constant for hyperoxidation of 12,000 M(-1) s(-1) and a rate constant

32 ess, Prxs can become inactivated through the hyperoxidation of an active site Cys residue to Cys sulp

33 Likewise, hyperoxidation of Cys(172)/Ser(172) mutant Prx I require

34 50 microM glutathione decreased post-anoxic hyperoxidation of NADH and improved electrical recovery

35 Hyperoxidation of peroxiredoxins can only occur efficien

36 we developed a simple assay to quantify the hyperoxidation of peroxiredoxins.

37 Hyperoxidation of Prx I was also detected in HeLa cells

38 During normal mitogenic signaling, hyperoxidation of PrxI and -II was not detected.

39 endent cell cycle arrest was correlated with hyperoxidation of PrxII, which resulted in quantitative

40 nation after anoxia in hippocampal slices is hyperoxidation of the electron carriers of the mitochond

41 ation after anoxia in hippocampal slices, is hyperoxidation of the electron carriers of the mitochond

42 We have found that hyperoxidation of the ER is prevented by attenuation of

43 e show that Ero1alpha hyperactivity leads to hyperoxidation of the ER oxidoreductase ERp57 and induce

44 ypothesized that Ccp1's heme is labilized by hyperoxidation of the protein during the burst in H2O2 p

45 Consequently, we reveal that the hyperoxidation of Tpx1 is critical to allow thioredoxin

46 Tsa1 and Hsp70 physically interact and that hyperoxidation of Tsa1 by H2O2 is required for the recru

47 diate is key to determine the probability of hyperoxidation or disulfide formation.

48 n cytosolic calcium overload and post-anoxic hyperoxidation (PAMHo) has been suggested in previous st

49 This "hyperoxidation" phenotype could be duplicated by incubat

50 A similar hyperoxidation rate constant for Prx3 was measured, but

51 ns of H2O2 concomitantly induce DJ-1 Cys-106 hyperoxidation (sulfination or sulfonation) in myocytes,

52 Prx disulfide formation and protect against hyperoxidation to the sulfinic acid.

53 Peroxiredoxin hyperoxidation was associated with inhibition of pro-sur

54 The intensity of NADH hyperoxidation was not significantly different among gro

55 Peroxiredoxin hyperoxidation was observedin situin human cartilage sec

56 Earlier studies suggested that mitochondrial hyperoxidation was produced by an oxyradical mechanism a

57 To identify the pathway responsible for ER hyperoxidation, we individually depleted several enzymes

58 Conversely, preventing cellular hyperoxidation with N-acetyl cysteine partially negated