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Originally published In Press as doi:10.1074/jbc.M202679200 on June 5, 2002

J. Biol. Chem., Vol. 277, Issue 33, 30253-30263, August 16, 2002
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A Novel Transactivating Factor That Regulates Interferon-gamma -dependent Gene Expression*

Junbo HuDagger §, Qingjun MengDagger , Sanjit K. RoyDagger , Abhijit Raha, Jiadi Hu, Jun Zhang, Katsuyuki Hashimoto, and Dhananjaya V. Kalvakolanu||

From the Marlene and Stewart Greenebaum Cancer Center, Department of Microbiology and Immunology, Molecular and Cellular Biology Program, University of Maryland School of Medicine, Baltimore, Maryland 21201 and the  Division of Genetic Resources, National Institute of Infectious Diseases, Tokyo 162-8640, Japan

We have previously identified a novel interferon (IFN)-stimulated cis-acting enhancer element, gamma -IFN-activated transcriptional element (GATE). GATE differs from the known IFN-stimulated elements in its primary sequence. Preliminary analysis has indicated that the GATE-dependent transcriptional response requires the binding of novel transacting factors. A cDNA expression library derived from an IFN-gamma -stimulated murine macrophage cell line was screened with a 32P-labeled GATE probe to identify the potential GATE-binding factors. A cDNA coding for a novel transcription-activating factor was identified. Based on its discovery, we named it as GATE-binding factor-1 (GBF-1). GBF-1 homologs are present in mouse, human, monkey, and Drosophila. It activates transcription from reporter genes carrying GATE. It possesses a strong transactivating activity but has a weak DNA binding property. GBF-1 is expressed in most tissues with relatively higher steady-state levels in heart, liver, kidney, and brain. Its expression is induced by IFN-gamma treatment. GBF-1 is present in both cytosolic and nuclear compartments. These studies thus identify a novel transactivating factor in IFN signaling pathways.

* This work was supported by Grants CA71401 and CA78282 from the NCI, National Institutes of Health (to D. V. K.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger These authors contributed equally to this work.

§ Present address: Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Peoples Republic of China.

|| To whom correspondence should be addressed: Greenebaum Cancer Center, University of Maryland School of Medicine, 655 W. Baltimore St., BRB 9th Floor, Baltimore, MD 21201.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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