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Overexpression of mitochondrial Trx2 attenuates the intracellular ROS accumulation and ATP production. Most interestingly, mitochondrial Trx2 may be involved in the cardiac hypertrophy signaling of diabetes.
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Prx3 and Trx2 comprise an adaptive system to sense changes in atmospheric oxygen tension and influence cellular injury responses through both detoxification of mitochondrial oxidants and regulation of mitochondrial redox-dependent signaling
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Trx2 overexpression failed to attenuate hypoxia-induced human pulmonary arterial smooth muscle cells proliferation in vitro or hypoxia-induced Pulmonary hypertension in vivo.
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study demonstrated that miR-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 expression through posttranscriptional gene silencing.
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No evidence that SNPs in TRX2 have effects, but the rs4485648 polymorphism of the TrxR2 gene might exert an independent effect on the development of Diabetic retinopathy.
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Thioredoxin 2 Is a Novel E2-Interacting Protein That Inhibits the Replication of Classical Swine Fever Virus by promoting the nuclear translocation of the p65 subunit of NF-kappaB.
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The Grx2 system could help to keep Trx2/1 reduced during an oxidative stress, thereby contributing to the anti-apoptotic signaling.
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CERKL interacts with TRX2 and plays a novel key role in the regulation of the TRX2 antioxidant pathway.
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TGF-beta-mediated expression of the epithelial-mesenchymal transition marker fibronectin was inhibited not only by chemicals that interfere with reactive oxygen species signaling but also by exogenously expressed mitochondrial thioredoxin.
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We showed that overexpression of TRXs reduced cell death; TRX2 was expressed in the mitochondria, while TRX1 was expressed in the cytoplasm.
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knockdown of TRX-1 or TRX-2 sensitizes cells to CYP2E1-induced oxidant stress partially via ASK-1 and JNK1 signaling pathways. Both TRX-1 and TRX-2 are important for defense against CYP2E1-induced oxidative stress.
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Data show that knockdown of S100P led to downregulation of thioredoxin 1 and beta-tubulin and upregulation of RhoGDIA, all potential therapeutic targets in cancer.
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TRX1 and TRX2 regulate the proliferation and survival of adipocyte derived stem cells; these processes are mediated by the activation of ERK1/2
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Both thioredoxin 2 and glutaredoxin 2 contribute to the reduction of the mitochondrial 2-Cys peroxiredoxin Prx3.
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mitochondrial thioredoxin may play important roles in protection against oxidant-induced apoptosis
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MT-TRX has a role in the regulation of the mitochondrial membrane potential and cell death
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Thioredoxin 1 and thioredoxin 2 have opposed regulatory functions on hypoxia-inducible factor-1alpha.
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The additive protection by Trx2 and GSH shows that Trx2 and GSH systems are both functionally important at low oxidative stress conditions.
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The LC/ICPMS analyses showed that the trivalent arsenic species were able to form complexes with both human and E. coli Trx.
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upon stimulation of Fas, thioredoxin-2 mediated denitrosylation of mitochondria-associated caspase-3, a process required for caspase-3 activation, and promoted apoptosis
