期刊
NUCLEIC ACIDS RESEARCH
卷 29, 期 17, 页码 3495-3505出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/29.17.3495
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We have characterized a 700 bp enhancer element around -6 kb relative to the HNF4 alpha1 transcription start. This element increases activity and confers glucocorticoid induction to a heterologous as well as the homologous promoters in differentiated hepatoma cells and is transactivated by HNF4 alpha1, HNF4 alpha7, HNF1 alpha and HNF1 beta in dedifferentiated hepatoma cells. A 240 bp sub-region conserves basal and hormone-induced enhancer activity. It contains HNF1, HNF4, HNF3 and C/EBP binding sites as shown by DNase I footprinting and electrophoretic mobility shift assays using nuclear extracts and/or recombinant HNF1 alpha and HNF4 alpha1. Mutation analyses showed that the HNF1 site is essential for HNF1 alpha transactivation and is required for full basal enhancer activity, as is the C/EBP site. Glucocorticoid response element consensus sites which overlap the C/EBP, HNF4 and HNF3 sites are crucial for optimal hormonal induction. We present a model that accounts for weak expression of HNF4 alpha1 in the embryonic liver and strong expression in the newborn/adult liver via the binding sites identified in the enhancer.
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