PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17015265-5 2006 While dissociation of the complex implies Trx oxidation, protein electrophoretic mobility shift assay detected oxidation of Trx only after bolus H2O2 but not after ADP stimulation. Hydrogen Peroxide 145-149 thioredoxin 1 Rattus norvegicus 124-127 16675629-8 2006 Oxidative stress in vitro (H2O2 in C2C12 myoblasts and myotubes) results in different changes: TrxR2, Trx2, and Trx1 are induced without alterations in the cytosolic thioredoxin reductase isoforms. Hydrogen Peroxide 27-31 thioredoxin 1 Rattus norvegicus 166-177 17015265-6 2006 These results demonstrate that the ADP-stimulated respiratory burst activated the ASK1-MKK4-JNK1/c-Jun signaling pathway in AM and suggest that transient and localized oxidation of Trx by the NADPH oxidase-mediated generation of H2O2 may play a critical role in ASK1 activation and the inflammatory response. Hydrogen Peroxide 229-233 thioredoxin 1 Rattus norvegicus 181-184 12878175-3 2003 The TRX gene conferred resistance to oxidative stress, such as hydrogen peroxide treatment, on the host hepatocytes. Hydrogen Peroxide 63-80 thioredoxin 1 Rattus norvegicus 4-7 11697114-6 2001 Moreover, exogenous recombinant wild type TRX decreased 51Cr release from primary cultured rat gastric mucosal cells incubated with ethanol or hydrogen peroxide in a dose-dependent manner, whereas recombinant mutant TRX (C32S/C35S), in which the two cysteines were replaced with serines in its active site, did not. Hydrogen Peroxide 143-160 thioredoxin 1 Rattus norvegicus 42-45 12011048-6 2002 Vitamin D(3)-up-regulated protein-1 down-regulation by strain or hydrogen peroxide led to increased thioredoxin activity, whereas adenovirus-mediated overexpression of vitamin D(3)-up-regulated protein-1 suppressed thioredoxin activity. Hydrogen Peroxide 65-82 thioredoxin 1 Rattus norvegicus 100-111 12643619-11 2003 Transient oxidative stress exerted by the addition of oxidative reagents diamide and hydrogen peroxide partially suppressed the growth of TRX-transfected cells. Hydrogen Peroxide 85-102 thioredoxin 1 Rattus norvegicus 138-141 11350800-1 2001 Peroxiredoxin I (Prx I) and peroxiredoxin II (Prx II) are found in abundance in the cytoplasm of cells and catalyze the reduction of hydrogen peroxide with the use of electrons provided by thioredoxin. Hydrogen Peroxide 133-150 thioredoxin 1 Rattus norvegicus 189-200 26346161-5 2015 Cell viability assay demonstrated that incubation with H2O2 for 24 h led to a significant loss of cultured rat PC12 cells, and the cell viability was pronouncedly increased by pretreatment of gensenoside Rb1 for 24 h. H2O2-induced endoplasmic reticulum stress pathway was also suppressed after gensenoside Rb1 pretreatment, which was related with thioredoxin-1 (Trx-1) induction. Hydrogen Peroxide 55-59 thioredoxin 1 Rattus norvegicus 347-360 8139268-2 1994 ADF/thioredoxin has several biologic functions, such as defense against cellular damage, activity to scavenge oxidative stress by hydrogen peroxide radicals and cytokine-like properties. Hydrogen Peroxide 130-147 thioredoxin 1 Rattus norvegicus 4-15 32160414-0 2020 Thioredoxin mitigates H2 O2 -induced inhibition of myogenic differentiation of rat bone marrow mesenchymal stem cells by enhancing AKT activation. Hydrogen Peroxide 22-27 thioredoxin 1 Rattus norvegicus 0-11 31823698-2 2019 The proteins of the thioredoxin (Trx) family are crucial mediators of protein function regulating the intracellular hydrogen peroxide levels and redox-sensitive post-translational protein changes. Hydrogen Peroxide 116-133 thioredoxin 1 Rattus norvegicus 20-31 31823698-2 2019 The proteins of the thioredoxin (Trx) family are crucial mediators of protein function regulating the intracellular hydrogen peroxide levels and redox-sensitive post-translational protein changes. Hydrogen Peroxide 116-133 thioredoxin 1 Rattus norvegicus 33-36 29989791-3 2018 In this study, we reported that Hon attenuates the H2O2- or 6-hydroxydopamine (6-OHDA)-induced apoptosis of PC12 cells by increasing the glutathione level and upregulating a multitude of cytoprotective proteins, including heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, thioredoxin 1, and thioredoxin reductase 1. Hydrogen Peroxide 51-55 thioredoxin 1 Rattus norvegicus 274-287 10513609-2 1999 The glutathione S-transferase and thioredoxin reductase activities and SH content decreased dose-dependently with H2O2, but thioredoxin activity increased at low H2O2 concentrations. Hydrogen Peroxide 114-118 thioredoxin 1 Rattus norvegicus 34-45 30387809-8 2019 Furthermore, NAC pretreatment decreased H2O2-induced phosphorylation of apoptosis signal-regulating kinase 1, which depends on the redox state of Trx1, and increased H2O2-induced phosphorylation of protein kinase B, which is essential to cell survival. Hydrogen Peroxide 40-44 thioredoxin 1 Rattus norvegicus 146-150 27101737-0 2016 The thioredoxin and glutathione-dependent H2O2 consumption pathways in muscle mitochondria: Involvement in H2O2 metabolism and consequence to H2O2 efflux assays. Hydrogen Peroxide 107-111 thioredoxin 1 Rattus norvegicus 4-15 27101737-0 2016 The thioredoxin and glutathione-dependent H2O2 consumption pathways in muscle mitochondria: Involvement in H2O2 metabolism and consequence to H2O2 efflux assays. Hydrogen Peroxide 107-111 thioredoxin 1 Rattus norvegicus 4-15 26346161-5 2015 Cell viability assay demonstrated that incubation with H2O2 for 24 h led to a significant loss of cultured rat PC12 cells, and the cell viability was pronouncedly increased by pretreatment of gensenoside Rb1 for 24 h. H2O2-induced endoplasmic reticulum stress pathway was also suppressed after gensenoside Rb1 pretreatment, which was related with thioredoxin-1 (Trx-1) induction. Hydrogen Peroxide 55-59 thioredoxin 1 Rattus norvegicus 362-367 26346161-5 2015 Cell viability assay demonstrated that incubation with H2O2 for 24 h led to a significant loss of cultured rat PC12 cells, and the cell viability was pronouncedly increased by pretreatment of gensenoside Rb1 for 24 h. H2O2-induced endoplasmic reticulum stress pathway was also suppressed after gensenoside Rb1 pretreatment, which was related with thioredoxin-1 (Trx-1) induction. Hydrogen Peroxide 218-222 thioredoxin 1 Rattus norvegicus 347-360 26346161-5 2015 Cell viability assay demonstrated that incubation with H2O2 for 24 h led to a significant loss of cultured rat PC12 cells, and the cell viability was pronouncedly increased by pretreatment of gensenoside Rb1 for 24 h. H2O2-induced endoplasmic reticulum stress pathway was also suppressed after gensenoside Rb1 pretreatment, which was related with thioredoxin-1 (Trx-1) induction. Hydrogen Peroxide 218-222 thioredoxin 1 Rattus norvegicus 362-367 22579569-2 2012 It has been suggested that Se acts through selenoproteins, of which thioredoxin reductase (TrxR) is relevant for reduction of harmful hydroperoxides and maintenance of thioredoxin (Trx) redox activity. Hydrogen Peroxide 134-148 thioredoxin 1 Rattus norvegicus 68-79 22579569-2 2012 It has been suggested that Se acts through selenoproteins, of which thioredoxin reductase (TrxR) is relevant for reduction of harmful hydroperoxides and maintenance of thioredoxin (Trx) redox activity. Hydrogen Peroxide 134-148 thioredoxin 1 Rattus norvegicus 91-94 23221719-3 2012 Here we provide evidence that the PPARgamma agonist RSG protects rat CMCs from hydrogen peroxide (H2O2)-induced apoptosis by TRx overexpression. Hydrogen Peroxide 79-96 thioredoxin 1 Rattus norvegicus 125-128 22366564-0 2012 Time course of hydrogen peroxide-thioredoxin balance and its influence on the intracellular signalling in myocardial infarction. Hydrogen Peroxide 15-32 thioredoxin 1 Rattus norvegicus 33-44 22366564-4 2012 Our results show that thioredoxin-1 appears to make an important contribution to the reduced H(2)O(2) concentration. Hydrogen Peroxide 93-101 thioredoxin 1 Rattus norvegicus 22-35 22585969-0 2012 Glutathione/thioredoxin systems modulate mitochondrial H2O2 emission: an experimental-computational study. Hydrogen Peroxide 55-59 thioredoxin 1 Rattus norvegicus 12-23 22585969-9 2012 Quantitatively, these results converge on the idea that GSH/Trx scavenging systems in mitochondria are both essential for keeping minimal levels of H(2)O(2) emission, especially during state 3 respiration, when the energetic output is maximal. Hydrogen Peroxide 148-156 thioredoxin 1 Rattus norvegicus 60-63 23221719-7 2012 This suggests that RSG protects rCMCs from H2O2-induced oxidative stress through TRx overexpression and a PPARgamma-dependent mechanism. Hydrogen Peroxide 43-47 thioredoxin 1 Rattus norvegicus 81-84 23221719-3 2012 Here we provide evidence that the PPARgamma agonist RSG protects rat CMCs from hydrogen peroxide (H2O2)-induced apoptosis by TRx overexpression. Hydrogen Peroxide 98-102 thioredoxin 1 Rattus norvegicus 125-128 20558743-0 2010 Respiration-dependent H2O2 removal in brain mitochondria via the thioredoxin/peroxiredoxin system. Hydrogen Peroxide 22-26 thioredoxin 1 Rattus norvegicus 65-76 23226354-2 2012 We have recently shown that isolated mitochondria consume hydrogen peroxide (H2O2) in a substrate- and respiration-dependent manner predominantly via the thioredoxin/peroxiredoxin (Trx/Prx) system. Hydrogen Peroxide 58-75 thioredoxin 1 Rattus norvegicus 154-165 23226354-2 2012 We have recently shown that isolated mitochondria consume hydrogen peroxide (H2O2) in a substrate- and respiration-dependent manner predominantly via the thioredoxin/peroxiredoxin (Trx/Prx) system. Hydrogen Peroxide 58-75 thioredoxin 1 Rattus norvegicus 181-184 23226354-2 2012 We have recently shown that isolated mitochondria consume hydrogen peroxide (H2O2) in a substrate- and respiration-dependent manner predominantly via the thioredoxin/peroxiredoxin (Trx/Prx) system. Hydrogen Peroxide 77-81 thioredoxin 1 Rattus norvegicus 154-165 23226354-2 2012 We have recently shown that isolated mitochondria consume hydrogen peroxide (H2O2) in a substrate- and respiration-dependent manner predominantly via the thioredoxin/peroxiredoxin (Trx/Prx) system. Hydrogen Peroxide 77-81 thioredoxin 1 Rattus norvegicus 181-184 23226354-9 2012 These data demonstrate that inhibition of the mitochondrial Trx/Prx system sensitizes dopaminergic cells to mitochondrial dysfunction, increased steady-state H2O2, and cell death. Hydrogen Peroxide 158-162 thioredoxin 1 Rattus norvegicus 60-63 23226354-10 2012 Therefore, in addition to their role in the production of cellular H2O2 the mitochondrial Trx/Prx system serve as a major sink for cellular H2O2 and its disruption may contribute to dopaminergic pathology associated with PD. Hydrogen Peroxide 67-71 thioredoxin 1 Rattus norvegicus 90-93 23226354-10 2012 Therefore, in addition to their role in the production of cellular H2O2 the mitochondrial Trx/Prx system serve as a major sink for cellular H2O2 and its disruption may contribute to dopaminergic pathology associated with PD. Hydrogen Peroxide 140-144 thioredoxin 1 Rattus norvegicus 90-93 20558743-8 2010 Differential oxidation of glutathione or thioredoxin proteins by copper (II) or arsenite, respectively, provided further support for the thioredoxin/peroxiredoxin system as the major contributor to mitochondrial H(2)O(2) removal. Hydrogen Peroxide 212-220 thioredoxin 1 Rattus norvegicus 41-52 20558743-8 2010 Differential oxidation of glutathione or thioredoxin proteins by copper (II) or arsenite, respectively, provided further support for the thioredoxin/peroxiredoxin system as the major contributor to mitochondrial H(2)O(2) removal. Hydrogen Peroxide 212-220 thioredoxin 1 Rattus norvegicus 137-148 20558743-9 2010 Inhibition of the thioredoxin system exacerbated mitochondrial H(2)O(2) production by the redox cycling agent, paraquat. Hydrogen Peroxide 63-71 thioredoxin 1 Rattus norvegicus 18-29 20558743-10 2010 Additionally, decreases in H(2)O(2) removal were observed in intact dopaminergic neurons with thioredoxin reductase inhibition, implicating this mechanism in whole cell systems. Hydrogen Peroxide 27-35 thioredoxin 1 Rattus norvegicus 94-105