Browse our anti-Thioredoxin 2 (TXN2) Antibodies

Human Thioredoxin 2 (TXN2) interaction partners

1. 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.

2. 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

3. Trx2 overexpression failed to attenuate hypoxia-induced human pulmonary arterial smooth muscle cells proliferation in vitro or hypoxia-induced Pulmonary hypertension in vivo.

4. study demonstrated that miR-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 expression through posttranscriptional gene silencing.

5. 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.

6. 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.

7. The Grx2 system could help to keep Trx2/1 reduced during an oxidative stress, thereby contributing to the anti-apoptotic signaling.

8. CERKL interacts with TRX2 and plays a novel key role in the regulation of the TRX2 antioxidant pathway.

9. 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.

10. We showed that overexpression of TRXs reduced cell death; TRX2 was expressed in the mitochondria, while TRX1 was expressed in the cytoplasm.

11. 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.

12. 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.

13. TRX1 and TRX2 regulate the proliferation and survival of adipocyte derived stem cells; these processes are mediated by the activation of ERK1/2

14. Both thioredoxin 2 and glutaredoxin 2 contribute to the reduction of the mitochondrial 2-Cys peroxiredoxin Prx3.

15. mitochondrial thioredoxin may play important roles in protection against oxidant-induced apoptosis

16. MT-TRX has a role in the regulation of the mitochondrial membrane potential and cell death

17. Thioredoxin 1 and thioredoxin 2 have opposed regulatory functions on hypoxia-inducible factor-1alpha.

18. The additive protection by Trx2 and GSH shows that Trx2 and GSH systems are both functionally important at low oxidative stress conditions.

19. The LC/ICPMS analyses showed that the trivalent arsenic species were able to form complexes with both human and E. coli Trx.

20. upon stimulation of Fas, thioredoxin-2 mediated denitrosylation of mitochondria-associated caspase-3, a process required for caspase-3 activation, and promoted apoptosis

Fruit Fly (Drosophila melanogaster) Thioredoxin 2 (TXN2) interaction partners

1. This is the first demonstration of biochemical and physiological consequences caused by loss of Trx-2 in Drosophila.

2. gene for thioredoxin (DmTrx-2) was cloned and expressed, and the protein characterized

3. Drosophila thioredoxin can function as an anti-aging agent and as a suppressor of Parkin-associated endothelin receptor-like receptor - and poly-glutamine-induced neurotoxicity

4. Trx-2 affects lifespan in Drosophila. Mutants have a decreased lifespan.

Mouse (Murine) Thioredoxin 2 (TXN2) interaction partners

1. The ventral signal observed from early stages colocalized with motor neuron markers Isl1/2 and FoxP1 and the strong ventral signal colocalizing with Isl1/2 was observed in all rostrocaudal segments of the spinal cord.

2. TRX-2 overexpression does not mitigate adverse effects of a high-calorie diet on synaptic plasticity

3. An essential role was identified for thioredoxin-2 in preserving cardiac function by suppressing mitochondrial reactive oxygen species.

4. The SirT1 regulates the expression of several antioxidant genes in bovine aortic endothelial cells, including Mn superoxide dismutase, catalase, peroxiredoxins 3 and 5, thioredoxin 2, thioredoxin reductase 2, and uncoupling protein 2.

5. This study shows that both fructose and glucose-sweetened liquid consumption results in fatty liver and upregulated thioredoxin-2 expression.

6. Both thioredoxin 2 and glutaredoxin 2 contribute to the reduction of the mitochondrial 2-Cys peroxiredoxin Prx3.

7. Data show that Nrf2 activity was increased in WT MEFs at the 0 or -46 mV conditions, but was inhibited in Trx2 Tg MEFs under the same conditions.

8. Homozygous mutant embryos do not survive to birth and die after implantation at Theiler stage 15/16.

9. the rapid E2-mediated activation of the Txn pathway is an important step in the response of the mammalian uterus to estrogen.

10. Trx2 is an endogenous regulator of the mitochondrial permeability transition.