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J Biol Chem, Vol. 275, Issue 4, 2986-2998, January 28, 2000
From the Most cancers originate as a result of aberrant
gene expression in mainly glandular epithelial tissues leading to
defects in epithelial cell differentiation. The latter is governed by
distinct sets of transcriptional regulators. Here we report the
characterization of epithelium-specific Ets factor, family member 3 (ESE-3), a novel member of the ESE subfamily of Ets transcription
factors. ESE-3 shows highest homology to two other epithelium
restricted Ets factors, ESE-1 and ESE-2. ESE-3, like ESE-1 and ESE-2,
is exclusively expressed in a subset of epithelial cells with highest expression in glandular epithelium such as prostate, pancreas, salivary
gland, and trachea. A potential role in branching morphogenesis is
suggested, since ESE-3 transactivates the c-MET promoter via three high
affinity binding sites. Additionally, ESE-3 binding to DNA sequences in
the promoters of several glandular epithelium-specific genes suggests a
role for ESE-3 in later stages of glandular epithelium differentiation.
Although ESE-3 and ESE-1 bind with similar affinity to various Ets
binding sites, ESE-3 and ESE-1 differ significantly in their ability to
transactivate the promoters containing these sites. Our results support
the notion that ESE-1, ESE-2, and ESE-3 represent a unique
epithelium-specific subfamily of Ets factors that have critical but
distinct functions in epithelial cell differentiation and proliferation.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF124438 (ESE-3a) and AF124439 (ESE-3b).
ESE-3, a Novel Member of an Epithelium-specific Ets Transcription
Factor Subfamily, Demonstrates Different Target Gene Specificity from
ESE-1*
§¶
,,,,,,,,
New England Baptist Bone and Joint
Institute, Beth Israel Deaconess Medical Center, and Harvard
Medical School, Boston, Massachusetts 02115, the
§ Laboratory for Molecular Oncology, Center for Human
Genetics, University of Leuven & Flanders Interuniversity Institute for
Biotechnology, Herestraat 49, B-3000 Leuven, Belgium, and
** Millennium Pharmaceuticals, Cambridge, Massachusetts 02139
*
This work was supported in part by National Institutes of
Health Grant RO1 CA76323 and a Brain Tumor Society research grant (both
to T. A. L.) and by National Institutes of Health Grant KO8/CA 71429 (to P. O.).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.
Both authors contributed equally to this work.
To whom correspondence should be addressed: New England Baptist
Bone and Joint Inst., Dept. of Medicine, Beth Israel Deaconess Medical
Center, Harvard Inst. of Medicine, 4 Blackfan Circle, Boston, MA 02115. Tel.: 617-667-3393; Fax: 617-975-5299; E-mail: tliberma@
caregroup.harvard.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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