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The X protein of the hepatitis B virus acts as a transcription factor when targeted to its responsive element.
Author(s) -
Unger T.,
Shaul Y.
Publication year - 1990
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1990.tb08315.x
Subject(s) - biology , transcription factor , virology , transcription (linguistics) , hepatitis b virus , microbiology and biotechnology , virus , genetics , gene , linguistics , philosophy
The X protein of hepatitis B virus (HBV) stimulates transcription of a large number of viral enhancers. This protein augments the activity of the HBV enhancer through a specific cis element, termed X responsive element (XRE). Multimers of XRE exhibit enhancer activity which is further stimulated by X. XRE binds multiple cellular transcription factors one of which is the C/EBP. We have constructed the DB gene containing the DNA‐binding domain of the C/EBP. This gene efficiently represses the enhancer activity of the XRE by competitive displacement of the XRE‐binding factors. Under these conditions, X was found to have only a partially stimulatory effect on transcription, suggesting that the XRE‐binding proteins are required for the activity of X. In contrast, an X‐DB hybrid protein that binds to the XRE is a strong transcription factor and acts without additional XRE‐binding proteins. Furthermore, studies of X mutants revealed that the carboxy‐terminus of the protein is required for this activation. These data show that X directly stimulates the cellular transcription machinery, possibly by protein‐protein interaction with the XRE‐binding factors.