Visit our FAQ
Toll Free Phone (USA and Canada Only): (888) 526-5351
Direct Phone: (734) 975-3888
Product Categories
Research Area
Application
Provide batch numbers separated by commas to download or request available product inserts, QC sheets, certificates of analysis, data packs, and GC-MS data.
Thioredoxin 2 (Trx2) is a thiol-disulfide oxidoreductase and part of the antioxidant thioredoxin system that is involved in the maintenance of cellular redox homeostasis.1 It is ubiquitously expressed, with the highest levels of expression in metabolically active tissues such as the heart, skeletal muscle, testis, kidney, adrenal gland, and brain, and is localized to the mitochondria.2,3 Trx2 contains two active site cysteine residues, but lacks the additional structural cysteines present in Trx1 that participate in dimerization.4 During the catalytic cycle, the active site cysteines are oxidized to a disulfide upon reduction of oxidized protein disulfide substrates and are subsequently restored to their reduced state by thioredoxin reductase (TrxR) and NADPH.1 Trx2 is upregulated by TNF-α and reactive oxygen species (ROS), inhibits TNF-α-induced NF-κB activation, and inhibits apoptosis through redox-sensitive binding and regulation of apoptosis signal-regulating kinase 1 (ASK1).5,6 Homozygous disruption of the gene encoding Trx2, Txn2, causes exencephaly and is embryonic lethal in mice.7 Trx2 deficiency is associated with premature neurodegeneration.8 Cayman’s Thioredoxin 2 Rabbit Monoclonal Antibody (Clone 054) can be used for immunohistochemistry (IHC).
WARNING This product is not for human or veterinary use.
1. The mitochondrial thioredoxin system. Antioxid. Redox Signal. 2(4), 801-810 (2000).
2. Cloning and expression of a novel mammalian thioredoxin. The Journal of Biological Chemisty 272(5), 2936-2941 (1997).
3. Expression of novel antioxidant thioredoxin-
4. Crystal structures of oxidized and reduced forms of human mitochondrial thioredoxin 2. Protein Sci. 14(10), 2610-2621 (2005).
5. Mitochondrial thioredoxin-
6. Thioredoxin-
7. The absence of mitochondrial thioredoxin 2 causes massive apoptosis, exencephaly, and early embryonic lethality in homozygous mice. Mol. Cell. Biol. 23(3), 916-922 (2003).
8. Human thioredoxin 2 deficiency impairs mitochondrial redox homeostasis and causes early-