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J Biol Chem, Vol. 273, Issue 12, 7030-7037, March 20, 1998
From the Department of Cell Biology, New York University Medical
Center, New York, New York 10016
The Tal1 oncogene is a class II basic
helix-loop-helix (bHLH) transcription factor, overexpressed in as much
as 60% of T cell acute lymphoblastic leukemia cases. Like other class
II bHLH proteins, Tal1 can heterodimerize with the class I bHLH
proteins, such as E47, and bind to a DNA recognition sequence termed E
box. Therefore, it is believed that the oncogenic capacity of Tal1 lies
in its ability, as a heterodimer with E47, to activate aberrantly a set of "leukemogenic" genes in T cells. However, compared with E47 homodimers, Tal1/E47 heterodimers are very poor transactivators. Thus
the effect of Tal1 is actually to inhibit E47 homodimer activity. Here
we propose that the transforming properties of Tal1 are the result of
its ability to inhibit E47 activity. We address the mechanism of Tal1
inhibition and demonstrate that Tal1/E47 heterodimers cannot activate
transcription because their respective activation domains are
incompatible. Furthermore, we present data showing that Tal1 can
inhibit E47-mediated activation of the CIP1 gene. Finally,
we demonstrate that Tal1 inhibits E47 activity in leukemic T cells.
The Tal1 Oncoprotein Inhibits E47-mediated Transcription
MECHANISM OF INHIBITION
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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