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Abstract
The unexpected paucity of human protein encoding genes suggested that polymorphisms altering gene expression might be more important than initially thought. From an evolutionary perspective, traits such as xenobiotic metabolism and transport that require a dynamic response to environmental changes would evolve more efficiently through variation in regulatory sequences versus coding variants. Such variation would be manifest as co-dominant traits and selection pressures would operate more efficiently because of their ability to impact fitness in the heterozygous state. Our current understanding of regulatory polymorphisms impacting drug disposition is reviewed including specific discussion regarding knowledge gaps and future research opportunities.
| ABBREVIATIONS | ||
| ADH: | = | Alcohol dehydrogenase |
| ALDH: | = | Aldehyde dehydrogenase |
| ARP-1: | = | Apoliprotein A regulatory protein |
| COUP-TF: | = | Chicken ovalbumin upstream promoter-transcription factor |
| CYP: | = | Cytochrome P450 |
| EPHX: | = | Epoxide hydrolase |
| FMO: | = | Flavin-containing monooxygenase |
| GST: | = | Glutathione S-transferase |
| MAF: | = | Minor allele frequency |
| MPA: | = | Mycophenolic acid |
| PXR: | = | Pregnane-x-receptor |
| SLC6A4: | = | Serotonin transporter |
| SN-38: | = | 7-ethyl-10-hydroxycamptothecin |
| SNP: | = | Single nucleotide polymorphism |
| SSRI: | = | Selective serotonin reuptake inhibitor |
| SULT: | = | Sulfotransferase |
| TPMT: | = | Thiopurine methyltransferase |
| UGT: | = | UDP glucuronosyltransferase |
| VNTR: | = | Variable number tandem repeat |