anti-Thioredoxin Reductase 2 (TXNRD2) Antikörper

Fruit Fly (Drosophila melanogaster) Thioredoxin Reductase 2 (TXNRD2) Interaktionspartner

1. mitochondrial and cytoplasmic variants are both essential for viability

Human Thioredoxin Reductase 2 (TXNRD2) Interaktionspartner

1. Based on recent research, it has been reported that the modulation of the Trx/TrxR system may be considered as a new target in the management of the metabolic syndrome, insulin resistance, and type 2 diabetes, as well as in the treatment of hypertension and atherosclerosis. In this review evidence about a possible role of this system as a marker of the metabolic syndrome is reported. [review]

2. TrxR2 was overexpressed in non-small-cell lung cancer cells; our results suggest that TrxR2 acts as an oncogenic gene in the context of lung cancer progression

3. p53R2 acts as a positive regulator of TrxR2 activity in mitochondria both under normal physiological conditions and during the cellular response to DNA damage

4. TrxR2 deficiency-induced impaired proliferation and death of chondrocytes may be the pathological mechanism of the osteoarthropathy due to Selenium deficiency.

5. Evidence that the rs4485648 polymorphism of the TrxR2 gene might exert an independent effect on the development of Diabetic retinopathy.

6. Data suggest that TXNRD2 may represent a druggable target that could be deployed to reduce the development of fatal pulmonary metastases in patients with osteosarcoma (OS).

7. A meta-analysis of the top SNPs identified three new associated loci in primary open angle glaucoma--TXNRD2, ATXN2, and FOXC1

8. The TXNRD2 rs 1548357 polymorphism might be a genetic risk factor for Myocardial infarction in subjects with T2 Diabetes mellitus of Slovenian origin.

9. Data suggest TXNRD1 and TXRNRD2 function at the top of a redox pyramid that governs the oxidation state of peroxiredoxins and other protein factors, thereby dictating a hierarchy of phenotypic responses to oxidative insults.

10. Absence of TXNRD2 in humans leads to glucocorticoid deficiency.

11. Single Nucleotide Polymorphisms in the genes GPX1 (rs1050450, rs1800668 and rs3811699), TrxR2 (rs5748469), and DIO2 (rs225014) may not be significantly associated with Kashin-Beck disease in a Tibetan population.

12. Development of subcutaneous fibrosis can be associated with genetic variation in the mitochondrial enzyme TXNRD2, critically involved in removal of ROS, and maintenance of the intracellular redox balance.

13. Data suggest that dietary factor (selenium supplementation) up-regulates endogenous antioxidant systems and protects trophoblasts from oxidative stress; selenium upregulates GPX1 (glutathione peroxidase 1) and thioredoxin reductases (TXNRD1; TXNRD2).

14. A role of GPx2, TrxR2 and TrxR3 in proliferation, apoptosis and, therefore, also during cancer development.

15. No obvious correlation can be found between rs5748469 polymorphisms in TrxR2 gene and the susceptibility to Kashin-Beck disease.

16. Mutation of this gene is involved in regulation of cellular redoc state in Dilated Cardiomyopathy.

17. study reveals significant differences between TrxR1 and TrxR2 in substrate specificity and metal compound inhibition in vitro and in cells

18. mammary tumors expressing the wild-type TR were readily suppressed by the IFN/RA combination. In contrast, the tumors bearing a mutant TR were resistant to regression.

19. Mitochondrial thioredoxin reductase and peroxiredoxin III are overexpressed in hepatocellular carcinomas.

20. Involvements of mitochondrial thioredoxin reductase in cell proliferation.

Mouse (Murine) Thioredoxin Reductase 2 (TXNRD2) Interaktionspartner

1. Maintenance of mitochondrial ROS via Txnrd2 in endothelial cells is necessary for an intact vascular homeostasis and remodeling. Txnrd2 plays a vitally important role in balancing mitochondrial ROS production in the endothelium.

2. Suggest role for Txnrd2 in sustaining heart function during aging and suggest that Txnrd2 may be a modifier of heart failure.

3. Regulatory link was discovered between mitochondrial Txnrd and the JNK-PHD2-Hif-1alpha axis, which highlights how the loss of Txnrd2 and the resulting altered mitochondrial redox balance impairs tumor growth as well as tumor-related angiogenesis.

4. Data suggest TXNRD1 and TXRNRD2 function at the top of a redox pyramid that governs the oxidation state of peroxiredoxins and other protein factors, thereby dictating a hierarchy of phenotypic responses to oxidative insults.

5. 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.

6. Data indicate that mammalian thioredoxin reductase (H-TrxR) reduces hypothiocyanous acid (HOSCN).

7. Txnrd2 exerts a crucial function during postischemic reperfusion via thiol regeneration.

8. Energization of mitochondria increases the antioxidant potential of the TrxR2/Trx2 system and that inhibition of TrxR2 results in increased H(2)O(2) emission.

9. Genomic organization and identification of a novel alternative splicing variant of mouse mitochondrial TrxR2 gene

10. Neither Trx2 nor TrxR2 gain of function modified the redox regulation of mitochondria-dependent apoptosis in cos-7 cells, Hela cells and Mouse Neuro2a cells.

11. Cardiac tissue-restricted ablation of thioredoxin reductase 2 results in fatal dilated cardiomyopathy

12. Results describe the crystal structures of oxidized and reduced mitochondrial thioredoxin reductase provide molecular details of the reaction mechanism.(

13. the function of TR3 is not limited to its role in Trx2 reduction

14. truncated enzyme/peptide substrate system examines the kinetics of the ring-opening step that occurs during the enzymatic cycle of TR. The ring-opening step is 300-500-fold slower when Sec is replaced with Cys in mTR3 when using this system

15. conditional Txnrd2 knockouts generated using CD4- and CD19Cre transgenic mice lack Txnrd2 expression in CD4-- and CD19-positive T- and B-lymphocytes, respectively.

16. The mechanism of the thiol/disulfide exchange step between the N- and C-terminal reaction centers of mitochondrial thioredoxin reductase was studied.

17. Transgenic mouse models for the vital selenoenzymes cytosolic thioredoxin reductase, mitochondrial thioredoxin reductase and glutathione peroxidase 4.