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A pharmacogenomic approach to therapy requires systematic knowledge of the regulatory regions of the genes, as well as basic understanding of transcriptional regulatory mechanisms of genes. Using the apolipoprotein (apo) A-I/CIII gene cluster as a model system, we have identified by  in vitro  and  in vivo  studies the regulatory elements and the factors which control its transcription. Studies in transgenic mice established that the hepatocyte nuclear factor (HNF-4) binding site of the apoCIII enhancer, which controls transcription of both genes, is required for the intestinal expression of  apoA-I  and  apoCIII  genes, and enhances synergistically their hepatic transcription  in vivo . The three Sp1 sites of the enhancer are also required for the intestinal expression of  apoA-I  and  apoCIII  genes  in vivo,  and for the enhancement of the hepatic transcription. The regulation of the apoE/apoCI/apoCIV/apoCII cluster is also cited. It is expected that identification of the regulatory regions of genes will be soon accelerated by the sequencing of several mammalian genomes. The functional analyses of the regulatory domains of genes involved in lipid homeostasis, combined with cross-species sequence comparisons in the near future, may identify natural regulatory gene polymorphisms in the general population that will permit rational pharmacogenomic approaches for treatment of dyslipidemias.

clinical chemistry and laboratory medicine

Regulatory Gene Mutations Affecting Apolipoprotein Gene Expression: Functions and Regulatory Behavior of Known Genes May Guide Future Pharmacogenomic Approaches to Therapy