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J Biol Chem, Vol. 274, Issue 40, 28075-28078, October 1, 1999

COMMUNICATION
p48 (ISGF-3) Is Involved in Interferon--induced Suppression of Hepatitis B Virus Enhancer-1 Activity

Kazuhiko Nakao, Keisuke Nakata^¶, Mayumi Yamashita, Youko Tamada, Keisuke Hamasaki^¶, Hiroki Ishikawa^¶, Yuji Kato^¶, Katsumi Eguchi^¶, and Nobuko Ishii

From the  Health Research Center and the  Department of Clinical Pharmacology, Nagasaki University and the ^¶ First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1, Sakamoto, Nagasaki 852-8501, Japan

Interferon- (IFN-) suppresses hepatitis B virus (HBV) gene expression by reducing its enhancer-1 activity. IFN- induces transcription factors, interferon-stimulated gene factor 3 (ISGF3), and interferon regulatory factor-1 (IRF-1), which activate interferon-inducible gene expression through binding to the interferon-stimulated regulatory element (ISRE) "AGTTTCNNTTTCNC" in the gene promoters. We found the ISRE-like sequence "AGGCTTTCACTTTCTC" in the HBV enhancer-1 region and elucidated the role of this sequence. Gel mobility shift assay showed binding of in vitro translated IRF-1 and in vitro translated p48 (ISGF3-), which is a component of ISGF3 to this sequence. However, nuclear extracts binding to this sequence from human hepatoma cells (HuH-7) treated with IFN- contained only the protein consisted of p48. In transfection experiments, IFN- suppressed the HBV enhancer-1 activity, and overexpression of p48 enhanced this inhibitory effect. Both mutation and deletion of the ISRE-like sequence in the HBV enhancer-1 region reduced the suppressive effect of IFN-. Our results suggest that the ISRE-like sequence in the HBV enhancer-1 can interact with the protein containing p48 and mediate the IFN--induced suppression of the enhancer activity.

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