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Molecular and Cellular Biology, February 2000, p. 1407-1418, Vol. 20, No. 4
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

A Novel TATA-Binding Protein-Binding Protein, ABT1, Activates Basal Transcription and Has a Yeast Homolog That Is Essential for Growth

Tsukasa Oda,1 Kentaro Kayukawa,2 Hiroko Hagiwara,3 Henrik T. Yudate,1 Yasuhiko Masuho,1 Yasufumi Murakami,3 Taka-aki Tamura,2 and Masa-aki Muramatsu1,4,*

Helix Research Institute, Inc., Kisarazu-shi, Chiba 292-0812,1 Department of Biology, Faculty of Science, Chiba University, Inage-ku, Chiba 263-8522,2 Cellular Physiology Laboratory, The Institute of Physical and Chemical Research (RIKEN), Tsukuba-shi, Ibaraki 305-0074,3 and Department of Biological Cybernetics, Medical Research Institute, Tokyo Medical Dental University, Bunkyo-ku, Tokyo 113-8510,4 Japan

Received 21 June 1999/Returned for modification 25 October 1999/Accepted 22 November 1999

Identification of a novel mouse nuclear protein termed activator of basal transcription 1 (mABT1) that associates with the TATA-binding protein (TBP) and enhances basal transcription activity of class II promoters is described. We also identify mABT1 homologous counterparts in Caenorhabditis elegans and Saccharomyces cerevisiae and show the homologous yeast gene to be essential for growth. The mABT1 associated with TBP in HeLa nuclear extracts and with purified mouse TBP in vitro. In addition, ectopically expressed mABT1 was coimmunoprecipitated with endogenous TBP in transfected cells. More importantly, mABT1 significantly enhanced transcription from an adenovirus major late promoter in a reconstituted cell-free system. We furthermore demonstrate that mABT1 consistently enhanced transcription from a reporter gene with a minimal core promoter as well as from reporter genes with various enhancer elements in a cotransfection assay. Taken together, these results suggest that mABT1 is a novel TBP-binding protein which can function as a basal transcription activator.

* Corresponding author. Mailing address: Helix Research Institute, Inc., 1532-3 Yana, Kisarazu-shi, Chiba 292-0812, Japan. Phone: 81 (0)438-52-3966. Fax: 81 (0)438-52-3952. E-mail: mmasaaki{at}hri.co.jp.

Molecular and Cellular Biology, February 2000, p. 1407-1418, Vol. 20, No. 4
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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