Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1.
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-TXNRD2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Thioredoxin reductase 2 (TXNRD2) also known as TRXR2 is an important enzyme in the thioredoxin system. It has a mass of approximately 57 kDa and resides mainly in the mitochondria. TXNRD2 acts as a homodimer and contains a selenocysteine residue at its active site which is essential for its enzymatic activity. TXNRD2 is expressed ubiquitously but shows higher levels in tissues with high metabolic activity such as the heart muscle and brain. Its primary mechanical role involves the reduction of thioredoxin which in turn assists in reducing other proteins by cysteine thiol-disulfide exchange.
Biological function summary
TXNRD2 plays an important role in maintaining cellular redox balance and combating oxidative stress. It is part of the thioredoxin system which together with thioredoxin and thioredoxin peroxidase constitutes a defense against reactive oxygen species (ROS). TXNRD2 helps facilitate DNA synthesis and repair protein folding and the regulation of apoptosis. As a member of this protective complex TXNRD2 contributes to safeguarding cellular function under various stress conditions by modulating the reduction capacity of cells.
Pathways
TXNRD2 is importantly involved in the antioxidant defense and mitochondrial function pathways. In the antioxidant defense pathway it works in conjunction with the glutathione system to reduce ROS and repair oxidative damage. Additionally in mitochondrial function TXNRD2 collaborates with peroxiredoxins and other mitochondrial antioxidant systems to ensure the integrity of the electron transport chain and prevent oxidative damage within the mitochondria. TXNRD2 shares functional relations with proteins like thioredoxin 1 and peroxiredoxin 3 in these pathways.
TXNRD2 has significant implications in cardiovascular diseases and cancer. Mutations or dysregulation of TXNRD2 can lead to increased oxidative stress and myocardial dysfunction contributing to heart failure. Similarly altered TXNRD2 expression has been associated with tumor progression due to its role in managing cellular apoptosis and antioxidant defense allowing cancer cells to survive in oxidative environments. TXNRD2’s interactions with the protein NADPH oxidase highlight its involvement in these conditions where irregular ROS production exacerbates disease progression.
