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1 sbF interaction partner, Rv1676, a predicted peroxiredoxin.
2 removal was observed following oxidation of peroxiredoxin.
3 des and regulates the expression of the OhrA peroxiredoxin.
4 tic mechanism of Asp f3, a two-cysteine type peroxiredoxin.
5 tion status of tubulin, HSP90, TGF-beta, and peroxiredoxins.
6 mple assay to quantify the hyperoxidation of peroxiredoxins.
7 roxyperoxide reductase E (AhpE), among other peroxiredoxins.
8 entative of the major class of bacterial BCP peroxiredoxins.
9 ses, catalases, glutathione-peroxidases, and peroxiredoxins.
10 x homeostasis through reducing hyperoxidized peroxiredoxins.
11 xy-eicosatetraenoic acids also over-oxidized peroxiredoxins.
12 was associated with increased expression of peroxiredoxin 1 (P<0.05), peroxiredoxin 3 (P<0.01), and
13 igomers and shifts in isoelectric points for peroxiredoxin 1 (Prdx-1), Prdx-3, and Prdx-4 isoforms wi
19 re used to assess the effect of UVB on TOPK, peroxiredoxin 1 (Prx1), and apoptosis in RPMI7951 cells.
23 1s) and the antioxidant enzymes catalase and peroxiredoxin 1, which may influence antioxidant potenti
25 se-1, and cyclooxygenase-2 oxidize the 2-Cys-peroxiredoxins 1, 2, and 3 to their sulfinic and sulfoni
28 /SNO may affect the redox cycle of mammalian peroxiredoxin-1 (Prx1), a representative of the 2-Cys Pr
29 ically interacts with the antioxidant enzyme peroxiredoxin-1 (PRX1), protects it from proteasome-medi
30 (2) (mH(2)O(2)) acting via the redox sensor, peroxiredoxin-1, a thiol peroxidase with high reactivity
31 ation of primary antioxidant systems such as peroxiredoxins-1, heme oxygenase-1, and anti-apoptotic f
35 nduces CDK5/p25-dependent phosphorylation of peroxiredoxin 2 (Prx2), resulting in inhibition of its p
36 estigated interactions between PTP1B and the peroxiredoxin 2 (Prx2)/thioredoxin 1 (Trx1)/thioredoxin
37 y in vitro; during therapy, disulfide-linked peroxiredoxin 2 dimer did not accumulate in red blood ce
38 tropomyosin alpha4 p=0.0108), antioxidative (peroxiredoxin 2 p=0.0092), and anti-inflammatory effects
39 pical thioredoxin ACHT1 is oxidized by 2-Cys peroxiredoxin (2-Cys Prx) in Arabidopsis plants illumina
40 studies revealed the participation of 2-Cys peroxiredoxin (2-Cys PRX), a thiol-dependent peroxidase,
42 on of Cys-sulfinic acid derivatives of 2-Cys peroxiredoxins (2-Cys Prxs), has been shown to catalyze
44 alysis revealed that the antioxidant enzymes peroxiredoxin-2 (Prdx2) and heme oxygenase-1 were upregu
45 lammatory stimuli induce release of oxidized peroxiredoxin-2 (PRDX2), a ubiquitous redox-active intra
46 mitochondria to the cytosol was evidenced by peroxiredoxin-2 (Prx2) oxidation, and Prx3 collapse was
49 ased expression of peroxiredoxin 1 (P<0.05), peroxiredoxin 3 (P<0.01), and heme oxygenase-1 (HO-1) (P
50 e (Sod), glutathione peroxidase 4 (Gpx4) and peroxiredoxin 3 (Prdx3) that render them susceptible to
51 merase gamma, mitochondrial topoisomerase I, peroxiredoxin 3 and manganese superoxide dismutase--are
52 re, N-acetylcysteine increased the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose ti
60 unolabeling for markers of oxidative stress (peroxiredoxin-3/5) and for a lipid peroxidation product
62 The endoplasmic reticulum (ER)-localized peroxiredoxin 4 (PRDX4) supports disulfide bond formatio
64 llothionein 3 (Mt3), tetraspanin 2 (Tspan2), peroxiredoxin 4 (Prdx4), stathmin-like 2 (Stmn2), myelin
67 study examined the role of Akt signaling and peroxiredoxin 4 expression in human umbilical cord blood
69 cord blood cells converge on Akt to elevate peroxiredoxin 4 levels, and these effects contribute to
70 occlusion increased Akt phosphorylation and peroxiredoxin 4 protein expression while reducing proteo
72 edoxin 4 activity with Akt Inhibitor IV or a peroxiredoxin 4-neutralizing antibody, respectively, neg
73 , we show that the thiol-specific peroxidase peroxiredoxin-4 (Prdx4) directly regulates IL-1beta gene
75 s), NAD(P)H quinone oxidoreductase-1 (Nqo1), peroxiredoxin-4 (Prdx4), and serine peptidase inhibitor
77 e E1, PYGB, Pgm2), and antioxidant proteins (peroxiredoxin 5, ferritin heavy chain 1) following rapam
78 f four proteins (macrophage capping protein, peroxiredoxin 5, heterogeneous nuclear ribonucleoprotein
79 ther by crystallography or NMR for the human peroxiredoxin 5, their affinities were for the first tim
80 ynthase, sperm equatorial segment protein 1, peroxiredoxin-5, secretoglobin family 1D and glucose-6-p
81 Sperm of bulls was related to seminal plasma peroxiredoxin-5, spermadhesin-1 and the spermadhesin-1 x
86 o show that following opioid administration, peroxiredoxin 6 (PRDX6) is recruited to the opioid recep
87 holipase A2 (PLA2)activity of phosphorylated peroxiredoxin 6 (Prdx6) is required for activation of NA
88 how that opioid receptor activation recruits peroxiredoxin 6 (PRDX6) to the receptor-Galphai complex
92 opioid, and D2 dopamine receptors stimulates peroxiredoxin 6 (PRDX6)-mediated production of reactive
94 or of PRDX6 and suggest that co-targeting of peroxiredoxin 6 or modulating miR-371-3p expression toge
96 cs analysis, we found that uterine levels of peroxiredoxin-6 (PRDX6), a unique antioxidant, are signi
97 r BQ-123, or ROS scavenging after SDRT using peroxiredoxin-6 overexpression or the SOD mimetic tempol
98 transporter (EAAT-2), apo-J (Clusterin), and peroxiredoxin-6) are selectively expressed in astrocytes
101 roxidase and glutathione peroxidase, and the peroxiredoxin abundance were increased for ROS scavengin
102 s and their changes are closely connected to peroxiredoxin activity and function but so far have been
107 tributions of the sole catalase KatE and the peroxiredoxin AhpC produced by these strains in defense
109 rains is restored by a mutant (ahpC*) of the peroxiredoxin AhpC, converting it to a disulfide reducta
111 disulfide center of the antioxidant protein peroxiredoxin (AhpC) to detoxify ROS such as hydrogen pe
113 that mass spectrometry shows contained 2-Cys peroxiredoxin also formed and precedes the appearance of
114 ne, a residue that occurs in place of Pro in peroxiredoxins, also led to the formation of the cluster
115 acks with a putative antioxidant OsmC family peroxiredoxin, an indicator of oxidative stress derived
117 ing the thioredoxin peroxidase activity of a peroxiredoxin and increasing the hydrogen peroxide resis
118 two proteins with antioxidative properties (peroxiredoxin and superoxide dismutase), and three prote
119 chanism is similar to that of atypical 2-Cys peroxiredoxin and that selenocysteine allows SelS to sus
121 in reveals a fold typical of the 2-Cys class peroxiredoxins and a dimeric form with an intermolecular
122 were identified, including ATPase, clathrin, peroxiredoxins and enolase, which may provide clues to t
123 h wild-type and mutant strains deficient for peroxiredoxins and glutathione peroxidases were equally
124 H2O2 is under sophisticated fine control of peroxiredoxins and glutathione peroxidases with their ba
125 d that Sesn2 physically interacts with 2-Cys peroxiredoxins and Nrf2 albeit under different reductive
126 ting from nonlinearity of H2O2 scavenging by peroxiredoxins and our study reveals that this regulator
127 s, including cysteine-dependent peroxidases (peroxiredoxins) and proteases, only relatively few pK(a)
128 y on select proteins, including thioredoxin, peroxiredoxins, and other validated redox active protein
132 d out in this list, as the related cytosolic peroxiredoxins are known to form disulfides in the prese
136 ain the phenotypic differences, and identify peroxiredoxin as an important component of virulence in
137 including the redox proteins thioredoxin and peroxiredoxin, as well as the growth factor receptors IG
139 ctrometry, we recently reclassified one such peroxiredoxin, bacterioferritin comigratory protein (BCP
142 ssion of an antioxidative enzyme, 2-Cysteine peroxiredoxin (BxPrx), was elevated in B. xylophilus fol
143 ces cerevisiae Altogether, the processing of peroxiredoxins by Imp2 or Oct1 likely represents systems
146 demonstrate a clear physiological role for a peroxiredoxin chaperone and reveal a novel and unexpecte
149 ongs to the atypical 2-cysteine subfamily of peroxiredoxins, commonly referred to as bacterioferritin
158 typhimurium AhpC is a founding member of the peroxiredoxin family, a ubiquitous group of cysteine-bas
160 fatty acids (FA) desaturases do not require peroxiredoxins for their activity, nor does FAD4 require
161 ved the crystal structure of a typical 2-Cys peroxiredoxin from Leishmania in the dimeric (pH 8.5) an
162 Thiol peroxidases (Tpxs) are dimeric 2-Cys peroxiredoxins from bacteria that preferentially reduce
163 to those obtained for two typical 2-cysteine peroxiredoxins from Saccharomyces cerevisiae (5.4 and 6.
164 atalase (encoded by hktE) and a bifunctional peroxiredoxin-glutaredoxin (encoded by pdgX) in resistan
165 on these data, we conclude that catalase and peroxiredoxin-glutaredoxin are determinants of bacterial
167 porins and H(2) O(2) is removed by catalase, peroxiredoxin, glutathione peroxidase-like enzymes and a
168 circadian oscillations in the redox state of peroxiredoxin have been described as an additional non-t
171 and contribute to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism.
174 stimulation, the expression and oxidation of peroxiredoxin II (PrdxII), a critical antioxidant enzyme
181 tive oxygen species, oxidizing mitochondrial peroxiredoxin, inactivating AKT/mTOR/p70S6K signaling, a
182 l, Day et al. reveal a surprising benefit of peroxiredoxin inactivation at high H(2)O(2), showing tha
183 ans Srx1 was also found to be required for a peroxiredoxin-independent function in promoting fungicid
184 support the subdivision of the BCP family of peroxiredoxins into two classes based on their catalytic
185 tive cysteine, the resolving cysteine of BCP peroxiredoxins is not conserved across all members of th
186 the use of the approach to compare different peroxiredoxin isoforms and to identify mutations and sma
188 ein folding, which led to the discovery that peroxiredoxin IV (PRDX4) catalyzes a parallel oxidation
193 quence similarity 213, member A (FAM213A), a peroxiredoxin-like antioxidative protein, was repressed
194 spectrometry reveal that DJ-1 is an atypical peroxiredoxin-like peroxidase that scavenges H(2)O(2) th
198 These results show that the mitochondrial peroxiredoxin of P. falciparum occurs in both dimeric an
208 regulation of ROS/RNS is largely attended by peroxiredoxins (Prdxs) and their main reductants, thiore
210 rtile, and the deficiency or inactivation of Peroxiredoxins (PRDXs) is associated with human male inf
211 , peroxynitrite, and organic hydroperoxides, peroxiredoxins (Prdxs) represent a major potential prote
212 that peroxiredoxin 1 (Prx1), a member of the peroxiredoxin protein family, acts as a key mediator in
213 ediated by the membrane protein GDE2 and the peroxiredoxin protein Prdx1 that promotes neurogenesis.
216 e we show that oxidation-reduction cycles of peroxiredoxin proteins constitute a universal marker for
217 TXNRD1) and sulfiredoxin (SRXN1), suggesting peroxiredoxin proteins had been oxidized during monoHAA
218 t discovery of oxidation-reduction cycles of peroxiredoxin proteins, which persist even in the absenc
222 PC-mutation-positive colorectal cancer.2-Cys peroxiredoxin (Prx) enzymes are highly expressed in most
224 parasite Leishmania infantum, mitochondrial peroxiredoxin (Prx) exerts intrinsic ATP-independent cha
226 iscovery that the redox regulatory proteins, peroxiredoxin (Prx) I and Prx II are specific targets of
228 ivity in vitro Remarkably, the processing of peroxiredoxin (Prx) proteins by Oct1 appears to be an ev
230 terioferritin comigratory protein (BCP) is a peroxiredoxin (Prx) that catalyzes the reduction of H(2)
231 tive site cysteine of the antioxidant enzyme peroxiredoxin (Prx) to the sulfinic acid form, Prx-SO(2)
232 estingly, ACHT1 oxidation is driven by 2-Cys peroxiredoxin (Prx), which in turn eliminates peroxides.
234 This reaction is unique to the typical 2-Cys peroxiredoxins (Prx) and plays a role in peroxide-mediat
241 of the active site cysteine in typical 2-Cys peroxiredoxins (Prx) to sulfinic acid during oxidative s
244 st Oct1 could cleave the human mitochondrial peroxiredoxin Prx3 when expressed in Saccharomyces cerev
245 ed to oxidative stress resistance, including peroxiredoxin PrxA, in response to hydrogen peroxide.
248 reduces hyperoxidized 2-cysteine-containing peroxiredoxins (Prxs) and protects cells against oxidati
249 nt peroxidases, including 2-cysteine (2-Cys) peroxiredoxins (PRXs) and thylakoid ascorbate peroxidase
254 O2H) residues, the sulfinic forms of certain peroxiredoxins (Prxs) are selectively reduced by sulfire
255 st group, glutathione peroxidases (GPxs) and peroxiredoxins (Prxs) are the most widespread and abunda
258 ether with thioredoxin reductase 1 (TR1) and peroxiredoxins (Prxs) comprises a key redox regulatory s
266 4) and a thylakoid-associated redox protein, PEROXIREDOXIN Q (PRXQ), to produce wild-type levels of 1
267 e polarization to monitor dynamic changes in peroxiredoxin quaternary structure inside the crowded en
269 Our results present in vivo evidence of a peroxiredoxin regulating DE-cadherin-mediated adhesion.
270 The crystal structure of the mitochondrial peroxiredoxin reveals a fold typical of the 2-Cys class
274 Because of its evolutionary conservation, peroxiredoxin signaling might underlie a general princip
275 genases and cyclooxygenases may affect 2-Cys peroxiredoxin signaling, analogous to NADPH oxidases in
276 modulate the oligomeric transitions of 2-Cys peroxiredoxins such as redox state, post-translational m
277 provided further support for the thioredoxin/peroxiredoxin system as the major contributor to mitocho
282 P) of Escherichia coli, as an atypical 2-Cys peroxiredoxin that functions through the formation of an
284 xpressions of those genes encoding catalase, peroxiredoxin, thioredoxin and glutathione were highly i
285 indicate that at high tissue H2O2 levels the peroxiredoxin-thioredoxin antioxidant chain becomes over
286 This detoxification pathway utilizes the peroxiredoxin/thioredoxin antioxidant system, as selecti
287 ignificant upregulation of components of the peroxiredoxin/thioredoxin pathway and processes involved
288 ivity of the endoplasmic reticulum-localized peroxiredoxin to hyperoxidation compared with either the
289 d that mutation of the TxxC active site in a peroxiredoxin to the CxxC form could lead to coordinatio
290 ctional gain that allows mitochondrial 2-Cys peroxiredoxins to act as molecular chaperones when formi
292 nhibitor-like allergen (Tri a 39), and 1-cys-peroxiredoxin (Tri a 32), produced the maximal area unde
293 y enhances the expression of the thioredoxin/peroxiredoxin (Trx/Prx) system with the greatest effect
295 fungal meningoencephalitis and regulation of peroxiredoxins, Tsa1 and Tsa3, and thioredoxins, Trx1 an
298 creased expression of the antioxidant enzyme peroxiredoxin-V, and a non-significant trend towards dec
300 the highly abundant eukaryotic typical 2-Cys peroxiredoxin, whose oxidative stress-induced sulfinic a