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A study is being made of the hepatic nuclear factors 1 and 4 (HNF1 and HNF4). These are both liver enriched transcription factors which activate the transcription of a large number of liver expressed genes, such as albumin, alpha-antitrypsin, apolipoprotein A1, alpha- and beta-fibrinogen and clotting factor IX by binding to a specific deoxyribonucleic acid (DNA) site in the promoter/enhancer of their respective genes.
The most significant result to emerge, concerns the 'knock-out' of the HNF1 gene in mice, showing that the gene was essential for postnatal, but not prenatal, development. The cause of death cannot be ascertained precisely, but it is clear that phenylalanine hydroxylase is inactive. This should lead to new lines of enquiry, and hopefully a further understanding of the regulation of the phenylalanine hydroxylase gene in liver.
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