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Human Monoclonal TXNRD2 Primary Antibody for IP - ABIN532566
Mustacich, Powis: Thioredoxin reductase. in The Biochemical journal 2000
mitochondrial and cytoplasmic variants are both essential for viability
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]
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
p53R2 acts as a positive regulator of TrxR2 activity in mitochondria both under normal physiological conditions and during the cellular response to DNA damage
TrxR2 deficiency-induced impaired proliferation and death of chondrocytes may be the pathological mechanism of the osteoarthropathy due to Selenium deficiency.
Evidence that the rs4485648 polymorphism of the TrxR2 gene might exert an independent effect on the development of Diabetic retinopathy.
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).
A meta-analysis of the top SNPs identified three new associated loci in primary open angle glaucoma--TXNRD2, ATXN2, and FOXC1
The TXNRD2 rs 1548357 polymorphism might be a genetic risk factor for Myocardial infarction in subjects with T2 Diabetes mellitus of Slovenian origin.
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.
Absence of TXNRD2 in humans leads to glucocorticoid deficiency.
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.
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.
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).
A role of GPx2, TrxR2 and TrxR3 in proliferation, apoptosis and, therefore, also during cancer development.
No obvious correlation can be found between rs5748469 polymorphisms in TrxR2 gene and the susceptibility to Kashin-Beck disease.
Mutation of this gene is involved in regulation of cellular redoc state in Dilated Cardiomyopathy.
study reveals significant differences between TrxR1 and TrxR2 in substrate specificity and metal compound inhibition in vitro and in cells
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.
Mitochondrial thioredoxin reductase and peroxiredoxin III are overexpressed in hepatocellular carcinomas.
Involvements of mitochondrial thioredoxin reductase in cell proliferation.
Thioredoxin reductase (TR) is a dimeric NADPH-dependent FAD containing enzyme that catalyzes the reduction of the active site disulfide of thioredoxin and other substrates. TR is a member of a family of pyridine nucleotide-disulfide oxidoreductases and is a key enzyme in the regulation of the intracellular redox environment. Three thioredoxin reductase genes have been found that encode selenocysteine containing proteins. This gene partially overlaps the COMT gene on chromosome 22.
, thioredoxin reductase
, selenoprotein Z
, thioredoxin reductase 2, mitochondrial
, thioredoxin reductase 3
, thioredoxin reductase TR3
, thioredoxin reductase beta
, TR beta