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(Received for publication, June 18, 1996, and in revised form, September 6, 1996)
From the TAL1/SCL is a basic helix-loop-helix (bHLH)
oncoprotein that is expressed in several cell lines including many
hematolymphoid cells, but not in T- and B-lineage cells. The
TAL1 gene was originally discovered as being
transcriptionally activated by chromosomal rearrangements in T-cell
acute lymphoblastic leukemia (T-ALL). Here we have shown that TAL1 and
the ubiquitously expressed murine bHLH transcription factor ALF1 formed
heterodimers that, compared with ALF1 homodimers, had a more restricted
E-box specificity and bound preferentially to the
glucocorticoid-responsive E-box (Egre) motif
(AA
Volume 271, Number 49,
Issue of December 6, 1996
pp. 31463-31469
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,¶
and
Department of Molecular Biology and the
¶ Department of Medical Microbiology and Immunology, Aarhus
University, C. F. Møllers Allé 130, DK-8000 Aarhus C,
Denmark
GT). Overexpression of the dominant inhibitory HLH
protein Id1 in NIH3T3 cells reduced the transcriptional activity mediated by ALF1 homodimers, whereas the transcriptional activity mediated by TAL1/ALF1 heterodimers was resistant to Id overexpression. Our results show that ALF1 may serve as a dimerization partner for the
bHLH oncoprotein TAL1 and form a complex with a distinctive DNA binding
property. These findings support the hypothesis that the leukemic
characteristics of the TAL1 oncoprotein could be mediated by activation
of a set of target genes as heterodimeric complexes with ubiquitously
expressed bHLH transcription factors such as ALF1 and that a principal
role of TAL1 might be to neutralize an Id-mediated inactivation.
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