Thioredoxin 1 Rabbit Monoclonal Antibody (Clone 002)

Thioredoxin 1 (Trx1) is a thiol-disulfide oxidoreductase and part of the antioxidant thioredoxin system that is involved in the maintenance of cellular thiol redox homeostasis.^1,2,3 It is ubiquitously expressed, localizes primarily to the cytoplasm with some nuclear localization, and is upregulated in and released from cells under conditions of oxidative stress.^1,4,2 Trx1 contains two active site cysteine residues at positions 32 and 35, with additional cysteines at positions 62, 69, and 73.² 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.^1,2 It regulates redox-sensitive transcription factors including NF-κB, p53, and the glucocorticoid receptor, as well as inhibits apoptosis through redox-sensitive binding and regulation of apoptosis signal-regulating kinase 1 (ASK1).^4,2 Homozygous disruption of the gene encoding Trx1, Txn1, is embryonic lethal in mice.^5,1 Cayman's Thioredoxin 1 Rabbit Monoclonal Antibody (Clone 002) can be used for ELISA and Western blot (WB) applications.

WARNING This product is not for human or veterinary use.

1. Haendeler, J. Thioredoxin-1 and posttranslational modifications. Antioxid. Redox Signal. 8(9-10), 1723-1728 (2006).

2. Watanabe, R., Nakamura, H., Masutani, H., et al. Anti-oxidative, anti-cancer and anti-inflammatory actions by thioredoxin 1 and thioredoxin-binding protein-2. Pharmacol. Ther. 127(3), 261-270 (2010).

3. Berndt, C., Lillig, C.H., and Holmgren, A. Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: Implications for diseases in the cardiovascular system. Am. J. Physiol. Heart Circ. Physiol. 292(3), H1227-H1236 (2007).

4. Raffel, J., Bhattacharyya, A.K., Gallegos, A., et al. Increased expression of thioredoxin-1 in human colorectal cancer is associated with decreased patient survival. J. Lab. Clin. Med. 142(1), 46-51 (2003).

5. Matsui, M., Oshima, M., Oshima, H., et al. Early embryonic lethality caused by targeted disruption of the mouse thioredoxin gene. Dev. Biol. 178(1), 179-185 (1996).