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J. Biol. Chem., Vol. 280, Issue 30, 27783-27791, July 29, 2005

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FBI-1 Enhances Transcription of the Nuclear Factor-B (NF-B)-responsive E-selectin Gene by Nuclear Localization of the p65 Subunit of NF-B^*

Dong-Kee Lee**, Jae-Eun Kang, Hye-Jin Park, Myung-Hwa Kim, Tae-Hee Yim, Jung-Min Kim, Min-Kyu Heo, Kyu-Yeun Kim, Ho Jeong Kwon¶, and Man-Wook Hur||

From the Department of Biochemistry and Molecular Biology and the Institute of Genetic Sciences, BK21 Project for Medical Sciences, Yonsei University School of Medicine, 134 ShinChon-Dong, SeoDaeMoon-Ku, Seoul 120-752, Korea, the Department of Biological Sciences, Ewha Womans University, DaeHyun-Dong, Seoul 120-750, Korea, and the ^¶Department of Biological Engineering, Sejong University, KunJa-Dong, KwangJin-Ku, Seoul 143-747, Korea

The POZ domain is a highly conserved protein-protein interaction motif found in many regulatory proteins. Nuclear factor-B (NF-B) plays a key role in the expression of a variety of genes in response to infection, inflammation, and stressful conditions. We found that the POZ domain of FBI-1 (factor that binds to the inducer of short transcripts of human immunodeficiency virus-1) interacted with the Rel homology domain of the p65 subunit of NF-B in both in vivo and in vitro protein-protein interaction assays. FBI-1 enhanced NF-B-mediated transcription of E-selectin genes in HeLa cells upon phorbol 12-myristate 13-acetate stimulation and overcame gene repression by IB or IB. In contrast, the POZ domain of FBI-1, which is a dominant-negative form of FBI-1, repressed NF-B-mediated transcription, and the repression was cooperative with IB or IB. In contrast, the POZ domain tagged with a nuclear localization sequence polypeptide of FBI-1 enhanced NF-B-responsive gene transcription, suggesting that the molecular interaction between the POZ domain and the Rel homology domain of p65 and the nuclear localization by the nuclear localization sequence are important in the transcription enhancement mediated by FBI-1. Confocal microscopy showed that FBI-1 increased NF-B movement into the nucleus and increased the stability of NF-B in the nucleus, which enhanced NF-B-mediated transcription of the E-selectin gene. FBI-1 also interacted with IB and IB.

Received for publication, May 4, 2005

^* This work was supported by a National Research Laboratory research grant (to M.-W. H.) from the Korea Institute of Science & Technology Evaluation and Planning, the Korea Ministry of Science and Technology. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^** Current address: Baylor College of Medicine, Dept. of Medicine, Division of Diabetes, Endocrinology, and Metabolism, One Baylor Plaza, Houston, TX 77030.

^|| To whom correspondence should be addressed. Tel.: 82-2-361-5188; Fax: 82-2-312-5041; E-mail: mwhur2{at}yumc.yonsei.ac.kr.

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