Disease relevance of Foxa2

• Hepatocyte nuclear factor 3beta inhibits hepatitis B virus replication in vivo [1].

High impact information on Foxa2

• We find that liver nuclear extracts contain three major binding activities for this site, which we call HNF-3A, HNF-3B, and HNF-3C [2].
• Binding sites for hepatocyte nuclear factor 3 beta or 3 gamma and pancreas transcription factor 1 are required for efficient expression of the gene encoding pancreatic alpha-amylase [3].
• Glucagon gene expression is negatively regulated by hepatocyte nuclear factor 3 beta [4].
• The results have demonstrated that Kir6.2 promoter possesses two regions regulating the promoter activity: a Foxa2-binding site (-1364 to -1210) and an Sp1/Sp3-binding site (-1035 to -939) [5].
• The additional expression of Isl-1 in IEC-6 cells expressing Pdx-1 attenuated overexpression of Foxa2 protein and enhanced Kir6.2 expression [5].

Biological context of Foxa2

• Binding of Foxa2 to the 18-bp enhancer was demonstrated using electrophoretic mobility shift assays [6].
• The cell-specific DNA-protein complex was selectively competed by a series of Foxa2 DNA binding sites, and the addition of Foxa2 antiserum supershifted the complex [6].
• Interestingly, overexpression of Foxa2 activated the 18-bp enhancer in heterologous cells but only in the presence of the adjacent helix-loop-helix motif [6].

Anatomical context of Foxa2

• Likewise, a complex similar to that seen with extracts from thyroid C cell lines was generated using an extract from heterologous cells expressing recombinant Foxa2 [6].
• Unexpectedly, Foxa2 overexpression repressed activity in the CA77 thyroid C cell line, suggesting that Foxa2 may interact with additional cofactors [6].
• Our data implicate HNF-3 beta in the control of glucagon gene expression and strengthen the idea of endodermal origin of the islet cells [4].
• Role of hepatocyte nuclear factor-3 alpha and hepatocyte nuclear factor-3 beta in Clara cell secretory protein gene expression in the bronchiolar epithelium [7].
• Another (CD1E0.7), located at -753bp, revealed high homology with binding sites for the Ets family, the hepatocyte nuclear factor-3beta, or the nuclear factor of activated T cells [8].

Other interactions of Foxa2

• TTF-1, HNF-3beta, and SP-B proteins were decreased in lung homogenates of exposed rats with CDH [9].
• This study has conclusively identified hepatocyte nuclear factor 3beta (HNF-3beta), a liver-enriched member of the HNF-3/forkhead gene family, as the predominant purified protein that interacts with the FPV motif [10].

References