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J. Biol. Chem., Vol. 276, Issue 21, 18082-18089, May 25, 2001
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From the The lck gene encodes a
protein-tyrosine kinase that plays a key role in signaling
mediated through T cell receptor (TCR) and pre-TCR complexes.
Transcription of the lck gene is regulated by two
independent promoter elements: the proximal and distal promoters.
Previous studies employing transgenic mice demonstrated that the
sequence between
Identification and Characterization of a Transcriptional
Regulator for the lck Proximal Promoter*
§¶,§
,,
Division of Immunology, Department of
Microbiology and Immunology, the Institute of Medical Science, the
University of Tokyo, Minato-ku, Tokyo 108-8639, Japan, the ** Department
of Immunology, University of Washington, Seattle, Washington 98195, the
§§ Cutaneous Biology Research Center,
Massachusetts General Hospital, Harvard Medical School, Charlestown,
Massachusetts 02129, and ¶¶ AMGEN, Thousand
Oaks, California 91320
584 and 240 from the transcription start site in
the mouse lck proximal promoter is required for its
tissue-specific expression in the thymus. In this study, we demonstrate
that a Krüppel-like zinc finger protein, mt
(BFCOL1, BERF-1,
ZBP-89, ZNF148), previously cloned as a protein that binds to the
CD3
gene enhancer, binds to the 365 to 328 region of the
lck proximal promoter. mt is ubiquitously expressed in
various cell lines and mouse tissues. Overexpressed mt is more
active in T-lineage cells than B-lineage cells for transactivating
an artificial promoter consisting of the mt binding site and a TATA box. Activity of the lck proximal promoter was
significantly impaired by mutating the mt binding site or by
reducing mt protein expression level by using antisense mRNA.
Our results indicate that mt activity is regulated in a
tissue-specific manner and that mt is a critical transactivator for
the lck proximal promoter.
*
This work was supported in part by Special Coordination
Funds of the Ministry of Education, Culture, Sports, Science and
Technology, the Japanese Government.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.
To whom correspondence should be addressed. Tel.:
81-3-5449-5264; Fax: 81-3-5449-5407; E-mail:
takakis@ims.u-tokyo.ac.jp.
Supported by the Howard Hughes Medical Institute Predoctoral
Fellowship in Biological Science.
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