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Retinoid X Receptor RXRα Binds to and Trans-Activates the Hepatitis B Virus Enhancer

Bingfang Huan and Aleem Siddiqui
Proceedings of the National Academy of Sciences of the United States of America
Vol. 89, No. 19 (Oct. 1, 1992), pp. 9059-9063
Stable URL: http://www.jstor.org/stable/2360331
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Retinoid X Receptor RXRα Binds to and Trans-Activates the Hepatitis B Virus Enhancer
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Abstract

A retinoid X receptor (RXR) response element was located within the functionally defined hepatitis B virus (HBV) enhancer element. A short segment of the enhancer that contains this region has been shown with genetic analysis to play a key role in the regulation of enhancer function and to represent a major determinant of liver-specific activity. Both the full-length protein and the DNA-binding domain of the liver-specific receptor RXRα bound to the putative retinoic acid response element in the HBV enhancer. In vivo, an HBV enhancer-reporter gene construct responds to induction with retinoic acid when cotransfected with an RXRα expression vector. A single-base transition (G → A) in the HBV retinoic acid response element leads to a dramatic reduction both in the in vitro binding activity of RXRα and the in vivo activity of the HBV enhancer. Thus, retinoic acid and the RXRα are implicated as being significant determinants in the liver-specific regulation of HBV gene expression and the resultant disease pathogenesis.

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