Hepatocyte nuclear factor 4a

In addition to PXR and CAR, several other nuclear receptors, such as vitamin D receptor (VDR), hepatocyte nuclear factor 4a (HNF4a), peroxisome proliferator-activated receptors (PPARs), and farnesoid X receptor (FXR), have also been implicated in the regulation of xenobiotic enzymes and transporters [9-12], More recently, results from our lab have shown that the liver X receptor (LXR), a previously known sterol sensor, can also regulate the expression of phase II SULTs, such as the bile acid detoxifying hydroxysteroid sulfotransferase Sult2a9/2al [13] and the estrogen sulfotransferase (Est/Sultlel) [14],... 

Zhang, M. and J.Y. Chiang (2001). Transcriptional regulation of the human sterol 12a-hydroxylase gene (CYP8BI) Roles of hepatocyte nuclear factor 4a in mediating bile acid repression. J. Biol. Chem. 276, 41690 1699. 

Yang, Y, M. Zhang, G. Eggertsen, and JY. Chiang (2002). On the mechanism of bile acid inhibition of rat sterol 12a-hydroxylase gene CYP8BI) transcription Roles of a-fetoprotein transcription factor and hepatocyte nuclear factor 4a. Biochim. Biophys. Acta 1583, 63-73. 

Martinez-Jimenez CP, Gomez-Lechon MJ, Castell JV, Jover R (2006) Underexpressed coaclivators PGClalpha and SRCl impair hepatocyte nuclear factor 4a function and promote dedifferentiation in human hepatoma cells. J Biol Chem 281 29840-29849... 

PCD/DCoH pterin-4a-carbinolamine dehydratase/dimerization cofactor of hepatocyte nuclear factor-1 a... 

Liver Trovafloxacin was withdrawn from the European market because of Uver toxicity and acute liver failure in 1999, but it is still available under very strong restrictions in the USA. In experiments in isolated human hepatocytes trovafloxacin inhibited expression of hepatic nuclear factor-4a (HNF-4ot), which in turn suppressed the function of a network of genes that govern major metabolic processes, lipid and carbohydrate metabolism, and mitochondrial biol-ogy [78 ]. The author concluded that this is the probable underlying mechanism of trovafloxacin-induced hepatotoxicity. 

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