Detection of Thioredoxin Reductase 1/TRXR1 in HeLa Human Cell Line by Flow Cytometry. HeLa human cervical epithelial carcinoma cell line was stained with Mouse Anti-Human/Mouse/Rat Thioredoxin Reductase 1/TRXR1 APC‑conjugated Monoclonal Antibody (Catalog # IC7428A, filled histogram) or isotype control antibody (Catalog # IC002A, open histogram). To facilitate intracellular staining, cells were fixed with Flow Cytometry Fixation Buffer (Catalog # FC004) and permeabilized with Flow Cytometry Permeabilization/Wash Buffer I (Catalog # FC005). View our protocol for Staining Intracellular Molecules.
Preparation and Storage
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Protect from light. Do not freeze.
12 months from date of receipt, 2 to 8 °C as supplied.
Background: Thioredoxin Reductase 1/TRXR1
Thioredoxin reductase 1 (TRXR1) is an approximately 70 kDa member of the class-I pyridine nucleotide-disulfide oxidoreductase family. Human TRXR1 is 649 amino acids (aa) in length. Residues 151-152 constitute a propeptide that is deleted from the mature protein. Splicing variants produce five additional isoforms for human TRXR1. Isoform 2 has a 32 aa substitution for aa 107-138 and a deletion of aa 1-106. Isoform 3 has a deletion of aa 1-51 and a 49 aa substitution for aa 52-100. Isoform 4 is missing aa 1-98 and has a 3 aa substitution for aa 99-101. Isoform 5 has a deletion of aa 1-150. Residues 56-156 make up a glutaredoxin domain, and residues 520-632 constitute a pyridine nucleotide-disulphide oxidoreductase dimerization domain. In addition, there are three phosphotyrosines at positions 161, 163, and 281, and a selenocysteine at position 648. Human TRXR1 shares 74% and 70% aa sequence identity with mouse and rat TRXR1, respectively. Isoform 1 is involved in glutaredoxin activity as well as thioredoxin reductase activity, and it induces actin and tubulin polymerization, which leads to formation of cell membrane protrusions. Isoform 4 has been shown to enhance the transcriptional activity of the beta receptor only. Finally, isoform 5 mediates cell death induced by a combination of interferon-beta and retinoic acid. Isoform 1 is expressed mostly in the Leydig cells, but also in the ovary, spleen, heart, liver, kidney, and pancreas and in a number of cancer cell lines. Isoform 4 is widely expressed with highest levels in the kidney, uterus, testis, ovary, prostate, placenta, and fetal liver.