| ID | Sequence | Length | GC content |
|---|---|---|---|
| ACACGCGACUCCCACAAGGUUGCAGCCGGAGCCGCCCAGCUCACCGAGA… | 2521 nt | 0.4383 | |
| ACACGCGACUCCCACAAGGUUGCAGCCGGAGCCGCCCAGCUCACCGAGA… | 2419 nt | 0.4349 | |
| ACACGCGACUCCCACAAGGUUGCAGCCGGAGCCGCCCAGCUCACCGAGA… | 2407 nt | 0.4346 | |
| ACACGCGACUCCCACAAGGUUGCAGCCGGAGCCGCCCAGCUCACCGAGA… | 2305 nt | 0.4308 |
This gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a cytoplasmic 2-electron reductase. This FAD-binding protein forms homodimers and reduces quinones to hydroquinones. This protein's enzymatic activity prevents the one electron reduction of quinones that results in the production of radical species. Mutations in this gene have been associated with tardive dyskinesia (TD), an increased risk of hematotoxicity after exposure to benzene, and susceptibility to various forms of cancer. Altered expression of this protein has been seen in many tumors and is also associated with Alzheimer's disease (AD). Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq, Jul 2008] CIViC Summary for NQO1 Gene
A study in mice demonstrated that the NQO1 showed a more remarkable effect at a lower paraquat dose (0.02 mg) than a higher dose (0.04 mg) during the initial destructive phase of lung injury, though it did not meet the >2-fold change threshold for a significant marker [Tomita et al. DOI:10.1016/J.Tox.2006.12.005]. In a porcine model of bromine-induced skin burns, the NQO1 was significantly increased at 7 days post-exposure for both 45-second and 8-minute exposures, and it was identified as part of the NRF2-mediated oxidative stress signaling pathway [Price et al. DOI:10.1016/j.toxlet.2008.08.007]. In rats, hepatic gene expression profiling following burn injury identified the NQO1 as a significantly altered metabolism gene on day 1 post-injury [Jayaraman et al. DOI:10.1016/j.jss.2007.05.025].