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J Biol Chem, Vol. 274, Issue 42, 29984-29993, October 15, 1999
From the Herman B Wells Center for Pediatric Research, Section of
Pediatric Hematology/Oncology, and Departments of Pediatrics and
Biochemistry & Molecular Biology, Indiana University School of
Medicine, Indianapolis, Indiana 46202
Four transcriptional activating
cis-elements within the gp91phox promoter bind a
protein complex of similar mobility and binding specificity, denoted
BID (binding increased during differentiation). The intensity of BID
complexes increases upon myeloid cell differentiation, coincident with
induction of gp91phox expression, and BID competes with the
transcriptional repressor CDP for binding to each of these promoter
elements. To determine the identity of BID, an expression library was
ligand screened with the BID-binding site that surrounds the
YY1 Binds Five cis-Elements and Trans-activates
the Myeloid Cell-restricted gp91phox Promoter
145-base
pair (bp) region of the gp91phox promoter. One recovered factor
that exhibits the expected binding specificity is YY1, a ubiquitous
multifunctional transcription factor. BID complexes that form with the
four binding sites within the gp91phox promoter are disrupted
by YY1 antiserum, and a fifth YY1-binding site was detected in the
412-bp promoter region. Overexpression of YY1 in transient
co-transfection assays trans-activates a minimal promoter containing
two copies of the
145-bp binding site from the gp91phox
promoter. Neither the level of YY1 protein nor DNA binding activity increases during myeloid cell differentiation. These studies identify a
target gene of YY1 function in mature myeloid cells, and demonstrate that YY1 function can be controlled during myeloid development by the
modulation of a competing DNA-binding factor.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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