| ID | Sequence | Length | GC content |
|---|---|---|---|
| GCAGAGAGCAGCCGGGCUGCCAGCGCAUCAGGUGGGCUGAGUCGAUGGA… | 2553 nt | 0.6138 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGUUUCAUGAUCAACAUGGGAGACUC… | 2500 nt | 0.6096 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGUGGCAAUACGGUUGGACUAGAAGG… | 2544 nt | 0.6050 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGGUAUAAAGAAGAAACUCAGAGAUU… | 2919 nt | 0.5896 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGGUGAGUGCUAUCUUUCGCGGCGAC… | 2480 nt | 0.6113 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGGUGAGUGCUAUCUUUCGCGGCGAC… | 2783 nt | 0.6195 | |
| GCAGAGAGCAGCCGGGCUGCCAGCGUUUCAUGAUCAACAUGGGAGACUC… | 2446 nt | 0.6104 |
This gene encodes an endoplasmic reticulum membrane oxidoreductase that is essential for multiple metabolic processes, including reactions catalyzed by cytochrome P450 proteins for metabolism of steroid hormones, drugs and xenobiotics. The encoded protein has a flavin adenine dinucleotide (FAD)-binding domain and a flavodoxin-like domain which bind two cofactors, FAD and FMN, that allow it to donate electrons directly from NADPH to all microsomal P450 enzymes. Mutations in this gene cause a complex set of disorders, including apparent combined P450C17 and P450C21 deficiency, amenorrhea and disordered steroidogenesis, congenital adrenal hyperplasia and Antley-Bixler syndrome, that resemble those caused by defects in steroid metabolizing enzymes such as aromatase, 21-hydroxylase, and 17 alpha-hydroxylase. [provided by RefSeq, Aug 2020]
A study in humans demonstrated that major blunt trauma triggers a selective upregulation of oxidative enzyme transcripts in circulating leukocytes, with the POR being up-regulated after injury as it is responsible for synthesizing NADPH required for cytochrome P450-mediated oxidation reactions [Brandfellner et al. DOI:10.1097/SHK.0b013e31829de02f].