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1 otein folding needs to be regulated to avoid hyperoxidation.
2 ukaryotic peroxiredoxins by their reversible hyperoxidation.
3 entration of HCO(3) (-)/CO(2) (25 mm) on its hyperoxidation.
4 g to the protection of peroxiredoxin IV from hyperoxidation.
5 er, making it is more resistant than Prx2 to hyperoxidation.
6 onding Prx2 chimera became more resistant to hyperoxidation.
7               Prxs vary in susceptibility to hyperoxidation.
8 tive to inactivation by peroxide-induced Prx hyperoxidation.
9 l signaling and protects protein thiols from hyperoxidation.
10 e diglutathionylated products and suppresses hyperoxidation.
11  DJ-1 shows potentiated H2O2-induced Cys-106 hyperoxidation.
12  mitochondrial lipid peroxides trigger PRDX3 hyperoxidation, a posttranslational modification that co
13 t does not change the apparent mitochondrial hyperoxidation after anoxia.
14  the DJ-1 C106A mutant, which fully prevents hyperoxidation, also showed exacerbated cell death respo
15           Their activity can be regulated by hyperoxidation and consequent inactivation of the active
16 2-like protein with increased sensitivity to hyperoxidation and decreased ability to form the intermo
17 ength of anoxic depolarization can influence hyperoxidation and electrical activity recovery followin
18 icals in promoting post-anoxic mitochondrial hyperoxidation and electrical failure, and suggest that
19 er antioxidants could suppress mitochondrial hyperoxidation and improve electrical recovery after ano
20 uitous HCO(3) (-)/CO(2) pair stimulates Prx1 hyperoxidation and inactivation bears relevance to Prx1
21 evealed that HCO(3) (-)/CO(2) increases Prx1 hyperoxidation and inactivation both in the presence of
22  formation as a protection mechanism against hyperoxidation and inactivation.
23            We report here that mitochondrial hyperoxidation and synaptic activity in hippocampal slic
24  to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism.
25 der adults exhibited higher levels of PRX1-3 hyperoxidation basally and under conditions of oxidative
26 dition, Prx2 was more sensitive than Prx1 to hyperoxidation caused by both urate hydroperoxide and hy
27 plasmic reticulum-localized peroxiredoxin to hyperoxidation compared with either the cytosolic or mit
28 r processes that involve redox cycling, with hyperoxidation controlling structural transitions that a
29 d rate constants for disulfide formation and hyperoxidation for human recombinant Prx2 and Prx3 by an
30                Our findings suggest that the hyperoxidation generated by Ero1alpha-C104A/C131A is add
31 of eukaryotic 2-Cys peroxiredoxins (Prxs) by hyperoxidation has been proposed to promote accumulation
32 rx1) exhibited both decreased expression and hyperoxidation in response to mutant Htt expressed in ei
33          Each enzyme is equally sensitive to hyperoxidation in the presence of a robust recycling sys
34 expression of Prdx4 is highly susceptible to hyperoxidation in the presence of high glucose.
35                                              Hyperoxidation inactivates the Prx and is implicated in
36 intermediate from the catalytic cycle to the hyperoxidation/inactivation pathway.
37 d NADPH) was necessary, indicating that such hyperoxidation occurs only when Prx I is engaged in the
38   This gave a second order rate constant for hyperoxidation of 12,000 M(-1) s(-1) and a rate constant
39 ess, Prxs can become inactivated through the hyperoxidation of an active site Cys residue to Cys sulp
40                                    Likewise, hyperoxidation of Cys(172)/Ser(172) mutant Prx I require
41  50 microM glutathione decreased post-anoxic hyperoxidation of NADH and improved electrical recovery
42                                              Hyperoxidation of peroxiredoxins can only occur efficien
43  we developed a simple assay to quantify the hyperoxidation of peroxiredoxins.
44                                              Hyperoxidation of Prx I was also detected in HeLa cells
45           During normal mitogenic signaling, hyperoxidation of PrxI and -II was not detected.
46 endent cell cycle arrest was correlated with hyperoxidation of PrxII, which resulted in quantitative
47 3)-encapsulating nanogels (IrNG) through the hyperoxidation of resulting intracellular thiols using r
48 nation after anoxia in hippocampal slices is hyperoxidation of the electron carriers of the mitochond
49 ation after anoxia in hippocampal slices, is hyperoxidation of the electron carriers of the mitochond
50                           We have found that hyperoxidation of the ER is prevented by attenuation of
51 e show that Ero1alpha hyperactivity leads to hyperoxidation of the ER oxidoreductase ERp57 and induce
52 ypothesized that Ccp1's heme is labilized by hyperoxidation of the protein during the burst in H2O2 p
53             Consequently, we reveal that the hyperoxidation of Tpx1 is critical to allow thioredoxin
54  Tsa1 and Hsp70 physically interact and that hyperoxidation of Tsa1 by H2O2 is required for the recru
55 diate is key to determine the probability of hyperoxidation or disulfide formation.
56 n cytosolic calcium overload and post-anoxic hyperoxidation (PAMHo) has been suggested in previous st
57                                        This "hyperoxidation" phenotype could be duplicated by incubat
58                                    A similar hyperoxidation rate constant for Prx3 was measured, but
59 ast redox oscillations-characterized by diel hyperoxidation/reduction cycles of 2-Cys peroxiredoxins-
60 ns of H2O2 concomitantly induce DJ-1 Cys-106 hyperoxidation (sulfination or sulfonation) in myocytes,
61 II)alamin intermediate stranded and prone to hyperoxidation to hydroxocobalamin, which is recalcitran
62 a mixed disulfide intermediates or undergoes hyperoxidation to the sulfinic acid.
63  Prx disulfide formation and protect against hyperoxidation to the sulfinic acid.
64          The susceptibility of 2-Cys Prxs to hyperoxidation varies greatly and depends on structural
65                                Peroxiredoxin hyperoxidation was associated with inhibition of pro-sur
66                        The intensity of NADH hyperoxidation was not significantly different among gro
67                                Peroxiredoxin hyperoxidation was observedin situin human cartilage sec
68 Earlier studies suggested that mitochondrial hyperoxidation was produced by an oxyradical mechanism a
69   To identify the pathway responsible for ER hyperoxidation, we individually depleted several enzymes
70 had minimal effect on rates of oxidation and hyperoxidation, whereas Asp and Trp decreased both by ~1
71              Conversely, preventing cellular hyperoxidation with N-acetyl cysteine partially negated