|Reactivity||Human, Mouse, Rat|
|Calculated MW||30868 Da|
|Positive Control||Western blot: 3T3 cell lysate, rat kidney cell lysate|
|Application & Usage||Western blot: 1:200|
|Other Names||Azoreductase, DT-diaphorase, Menadione reductase, NAD (P) H, quinine oxidoreductase 1|
|Formulation||100 µg (0.5 mg/ml) of antibody in PBS, 0.01 % BSA, 0.01 % thimerosal, and 50 % glycerol, pH 7.2|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||NQO1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||The enzyme apparently serves as a quinone reductase in connection with conjugation reactions of hydroquinons involved in detoxification pathways as well as in biosynthetic processes such as the vitamin K-dependent gamma-carboxylation of glutamate residues in prothrombin synthesis.|
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Provided below are standard protocols that you may find useful for product applications.
NAD (P) H:quinone oxidoreductase 1 (NQO1) and NRH:quinone oxidoreductase (NQO2) are flavoproteins that catalyze the metabolic detoxification of quinones and their derivatives to hydroquinones, using either NADH or NADPH as the electron donor. This protects cells against quinone-induced oxidative stress, cytotoxicity, and mutagenicity. Many tumors overexpress NQO1, which is an obligate two-electron reductase that deactivates toxins and activates bioreductive anticancer drugs. NQO1, a 274 amino acid protein, is ubiquitously expressed, but the expression level varies among tissues. NQO1 gene expression is coordinately induced in response to xenobiotics, antioxidants, heavy metals and radiation. The antioxidant response element (ARE) in the NQO1 gene promoter is essential for expression and coordinated induction of NQO1. ARE activation by tert-butylhydroquinone is dependent on PI3-kinase, which lies upstream of Nrf2. Nrf2, c-Jun, Nrf1, Jun-B and Jun-D bind to the ARE and regulate expression and induction of NQO1 gene. Maf-Maf homodimers and possibly Maf-Nrf2 heterodimers play a role in negative regulation of ARE-mediated transcription, but Maf-Nrf1 heterodimers fail to bind with the NQO1 gene ARE and do not repress NQO1 transcription.
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