Thioredoxin (TRX) Antibody – Mouse Monoclonal

TXN: Participates in various redox reactions through the reversible oxidation of its active center dithiol to a disulfide and catalyzes dithiol-disulfide exchange reactions. Plays a role in the reversible S-nitrosylation of cysteine residues in target proteins, and thereby contributes to the response to intracellular nitric oxide. Nitrosylates the active site Cys of CASP3 in response to nitric oxide (NO), and thereby inhibits caspase-3 activity. Induces the FOS/JUN AP-1 DNA-binding activity in ionizing radiation (IR) cells through its oxidation/reduction status and stimulates AP-1 transcriptional activity. Homodimer; disulfide-linked. Interacts with TXNIP through the redox-active site. Interacts with MAP3K5 and CASP3. In case of infection, interacts with S.typhimurium protein slrP. Interacts with APEX1; the interaction stimulates the FOS/JUN AP-1 DNA- binding activity in a redox-dependent manner. Up-regulated by ionizing radiation. Belongs to the thioredoxin family.

Protein type: Nuclear receptor co-regulator

Chromosomal Location of Human Ortholog: 5q24

Cellular Component: axon; cell soma; cytoplasm; cytosol; dendrite; mitochondrion; nucleus

Molecular Function: enzyme binding; oxidoreductase activity, acting on sulfur group of donors, disulfide as acceptor; peptide disulfide oxidoreductase activity; protein disulfide oxidoreductase activity; protein-disulfide reductase activity; thioredoxin-disulfide reductase activity

Biological Process: cell redox homeostasis; negative regulation of protein export from nucleus; negative regulation of transcription from RNA polymerase II promoter; positive regulation of DNA binding; positive regulation of peptidyl-serine phosphorylation; regulation of protein import into nucleus, translocation; response to activity; response to axon injury; response to drug; response to radiation; response to selenium ion