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J. Biol. Chem., Vol. 276, Issue 12, 9421-9436, March 23, 2001
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From the New England Baptist Bone and Joint Institute, Beth Israel
Deaconess Medical Center, and Harvard Medical School,
Boston, Massachusetts 02115
We report here the isolation of
Tel-2, a novel member of the Ets transcription
factor family, with high homology to Tel/ETV-6. Tel-2 is
the second mammalian member of the Tel Ets family subclass whose
prototype Tel is involved in various chromosomal
translocations in human cancers. Six differentially expressed
alternative splice products of Tel-2 were characterized
encoding different Tel-2 isoforms which either contain or lack the
amino-terminal Pointed domain and also vary at the carboxyl terminus.
In contrast to Tel, which is highly expressed in several
different cell types and tissues, Tel-2 is only weakly
expressed in a variety of tissues and cell types, including placenta,
prostate, spleen, liver, and lung. Tel-2 binds to functionally relevant
Ets-binding sites of several genes and only the Tel-2 isoform
containing the Pointed domain and the DNA-binding domain acts as a
strong repressor of transcription. The retinoic acid
receptor The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF116508 (Tel-2a), AF116509 (Tel-2b), AF116510 (Tel-2c), AF218235 (Tel-2d), AF218365 (Tel-2e), and AF218366 (Tel-2f).
Tel-2 Is a Novel Transcriptional Repressor Related to the
Ets Factor Tel/ETV-6*
,,
and bone morphogenetic protein-6B
(BMP-6) genes are specifically repressed by Tel-2
indicating a function for Tel-2 as an inhibitor of differentiation. Due
to the important involvement of Tel in human cancer and the
location of Tel-2 within the MHC cluster region,
Tel-2 might be involved in chromosomal translocations in
human cancer as well.
*
This work was supported by National Institutes of Health
Grants RO1 CA76323 and CA72009 (to T. A. L.) and 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.
Contributed equally to the results of this work.
§
To whom correspondence should be addressed: New England Baptist
Bone & Joint Institute, Dept. of Medicine, Beth Israel Deaconess Medical Center, 4 Blackfan Circle, Boston, MA 02115. Tel.:
617-667-3393; Fax: 617-975-5299; E-mail:
tliberma@caregroup.harvard.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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