|Application ||WB, E|
|Isotype||Mouse IgG 1|
|Calculated MW||70906 Da|
|Positive Control||WB analysis of HeLa and Jurkat cell lysates.|
|Application & Usage||Western blot: 1:1000, IP: 1-2 µl, ELISA.|
|Other Names||Thioredoxin Reductase, GRIM-12, MGC9145, TR, TR1, TRXR1, TXNR.|
|Target/Specificity||Thioredoxin Reductase 1|
|Formulation||100 µl of antibody in HEPES with 0.15 M NaCl, 0.01 % BSA, 0.03 % sodium azide, and 50 % glycerol|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||Thioredoxin Reductase 1 Antibody (19A1) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Isoform 1 may possess glutaredoxin activity as well as thioredoxin reductase activity and induces actin and tubulin polymerization, leading to formation of cell membrane protrusions. Isoform 4 enhances the transcriptional activity of estrogen receptors alpha and beta while isoform 5 enhances the transcriptional activity of the beta receptor only. Isoform 5 also mediates cell death induced by a combination of interferon-beta and retinoic acid.|
|Cellular Location||Cytoplasm. Isoform 5: Cytoplasm.|
|Tissue Location||Isoform 1 is expressed predominantly in Leydig cells (at protein level). Also expressed in ovary, spleen, heart, liver, kidney and pancreas and in a number of cancer cell lines Isoform 4 is widely expressed with highest levels in kidney, testis, uterus, ovary, prostate, placenta and fetal liver|
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The mammalian thioredoxin reductases (TrxRs) are a family of seleno-cysteine containing pyridine nucleotide-disulfide oxido-reductases. All the mammalian TrxRs are homologous to glutathione reductase with respect to primary structure including the conserved redox catalytic site (-Cys-Val-Asn-Val-Gly-Cys-) but distinctively with a C-terminal extension containing a catalytically active penultimate seleno-cysteine (SeCys) residue in the conserved sequence(-Gly-Cys-SeCys-Gly). TrxR is homodimeric protein in which each monomer includes an FAD prosthetic group, a NADPH binding site and a redox catalytic site. Electrons are transferred from NADPH via FAD and the active-site disulfide to C-terminal SeCys-containing redox center, which then reduces the substrate like thioredoxin. The members of TrxR family are 55 – 58 kDa in molecular size and composed of three isoforms including cytosolic TrxR1, mitochondrial TrxR2, and TrxR3, known as Trx and GSSG reductase (TGR). TrxR plays a key role in protection of cells against oxidative stress and redox-regulatory mechanism of transcription factors and various biological phenomena. TrxR1 plays a central role as a glucosyl donor in cellular metabolic pathways.
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