ArticleMolecular and cellular biology1996
TFIIB-directed transcriptional activation by the orphan nuclear receptor hepatocyte nuclear factor 4.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 67 citations in OpenAlex.
- Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis.Nature communications · 2019Article
- Article
- PIC Activation through Functional Interplay between Mediator and TFIIH.Journal of molecular biology · 2017Article
- FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells.Cell stress & chaperones · 2017Article
- Global proteomic profiling reveals altered proteomic signature in schizophrenia serum.Molecular psychiatry · 2010Article
- Two functional modes of a nuclear receptor-recruited arginine methyltransferase in transcriptional activation.Molecular cell · 2006Article
- Negative autoregulation of HNF-4alpha gene expression by HNF-4alpha1.The Biochemical journal · 2005Article
- Repression of the luteinizing hormone receptor gene promoter by cross talk among EAR3/COUP-TFI, Sp1/Sp3, and TFIIB.Molecular and cellular biology · 2003Article
- TRAP/SMCC/mediator-dependent transcriptional activation from DNA and chromatin templates by orphan nuclear receptor hepatocyte nuclear factor 4.Molecular and cellular biology · 2002Article
- Competitive cofactor recruitment by orphan receptor hepatocyte nuclear factor 4alpha1: modulation by the F domain.Molecular and cellular biology · 2002Article
- Transcriptional activation by hepatocyte nuclear factor-4 in a cell-free system derived from rat liver nuclei.Nucleic acids research · 2001Article
- Hepatocyte nuclear factor 4alpha (nuclear receptor 2A1) is essential for maintenance of hepatic gene expression and lipid homeostasis.Molecular and cellular biology · 2001Article
- Modulation of transcriptional activation and coactivator interaction by a splicing variation in the F domain of nuclear receptor hepatocyte nuclear factor 4alpha1.Molecular and cellular biology · 1999Article
- Oestrogen receptor facilitates the formation of preinitiation complex assembly: involvement of the general transcription factor TFIIB.The Biochemical journal · 1998Article
- The activation function 2 domain of hepatic nuclear factor 4 is regulated by a short C-terminal proline-rich repressor domain.Nucleic acids research · 1998Article
- A dynamic model for PC4 coactivator function in RNA polymerase II transcription.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- An alternative splice variant of the tissue specific transcription factor HNF4alpha predominates in undifferentiated murine cell types.Nucleic acids research · 1998Article
- Hepatocyte nuclear factor 1alpha gene inactivation impairs chromatin remodeling and demethylation of the phenylalanine hydroxylase gene.Molecular and cellular biology · 1997Article
- Protein kinase A-dependent phosphorylation modulates DNA-binding activity of hepatocyte nuclear factor 4.Molecular and cellular biology · 1997Article
- Chicken ovalbumin upstream promoter transcription factors act as auxiliary cofactors for hepatocyte nuclear factor 4 and enhance hepatic gene expression.Molecular and cellular biology · 1997Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The orphan nuclear receptor hepatocyte nuclear factor 4 (HNF-4) is required for development and maintenance of the liver phenotype. HNF-4 activates several hepatocyte-specific genes, including the gene encoding apolipoprotein AI (apoAI), the major protein component of plasma high-density lipoprotein. The apoAI gene is activated by HNF-4 through a nuclear receptor binding element (site A) located in its liver-specific enhancer. To decipher the mechanism whereby HNF-4 enhances apoAI gene transcription, we have reconstituted its activity in a cell-free system. Functional HNF-4 was purified to homogeneity from a bacterial expression system. In in vitro transcription assays employing nuclear extract from HeLa cells, which do not contain HNF-4, recombinant HNF-4 stimulated transcription from basal promoters linked to site A. Activation by HNF-4 did not exhibit a ligand requirement, but phosphorylation of HNF-4 in the in vitro transcription system was observed. The activation function of HNF-4 was localized to a domain displaying strong homology to the conserved AF-2 region of nuclear receptors. Dissection of the transcription cycle revealed that HNF-4 activated transcription by facilitating assembly of a preinitiation complex intermediate consisting of TBP, the TATA box-binding protein component of TFIID and TFIID, via direct physical interactions with TFIIB. However, recruitment of TFIIB by HNF-4 was not sufficient for activation, since HNF-4 deletion derivatives lacking AF-2 bound TFIIB. On the basis of these results, HNF-4 appears to activate transcription at two distinct levels. The first step involves AF-2-independent recruitment of TFIIB to the promoter complex; the second step is AF-2 dependent and entails entry of preinitiation complex components acting downstream of TFIIB.
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