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Originally published In Press as doi:10.1074/jbc.M103893200 on May 30, 2001

J. Biol. Chem., Vol. 276, Issue 31, 28933-28938, August 3, 2001
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Inhibition of LZIP-mediated Transcription through Direct Interaction with a Novel Host Cell Factor-like Protein*

Hai-Jun ZhouDagger , Chi-Ming Wong§, Jian-He ChenDagger , Bo-Qin QiangDagger , Jian-Gang YuanDagger , and Dong-Yan Jin§||

From the Dagger  National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, and Peking Union Medical College, Chinese National Human Genome Center, Beijing 100005, China and the § Institute of Molecular Biology, The University of Hong Kong, Pokfulam Road, Hong Kong SAR, China

Host cell factor 1 (HCF-1) is a cellular transcriptional coactivator which coordinates the assembly of enhancer complex through direct interactions with viral and cellular trans-activators such as VP16, Oct-1, LZIP, and GA-binding protein. These interactions are mediated by the beta -propeller domain comprising the first 380 residues of HCF-1 with six kelch repeats. Here we describe the identification and characterization of a novel HCF-like kelch repeat protein, designated HCLP-1. HCLP-1 is a ubiquitously expressed nuclear protein which is composed almost entirely of a six-bladed beta -propeller. HCLP-1 selectively interacts with LZIP but not with VP16. The physical interaction between HCLP-1 and LZIP leads to the repression of the LZIP-dependent transcription. The HCLP-1-binding domain of LZIP maps to residues 109-315, which contain the bZIP DNA-binding motif. Electrophoretic mobility shift assay demonstrates that HCLP-1 indeed interferes with the binding of LZIP to its DNA target. Thus, HCLP-1 serves a transcriptional co-repressor function mediated through its inhibitory interaction with the LZIP transcription factor. Our findings suggest a new mechanism for transcriptional regulation by HCF-like proteins.

* This work was supported by Hong Kong Research Grants Council Grant N-HKU015/00 under NSFC/RGC JRS, University of Hong Kong Grant 10300147.32993.43700.305.01, National Natural Science Foundation of China Grants 39830070 and 3001161945, National Program for Key Basic Research Project G1998051002, and National High Technology R&D Program.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.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF113131 for HCLP-1.

To whom correspondence may be addressed. Tel.: 852-22990777; Fax: 852-28171006; E-mail: dyjin@hkucc.hku.hk or yuanjg@mail.east.net.cn.

|| Leukemia and Lymphoma Society Scholar.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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