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J. Biol. Chem., Vol. 276, Issue 7, 4597-4603, February 16, 2001
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From the Department of Pharmacology, University of Minnesota
Medical School, Minneapolis, Minnesota 55455-0217
The mouse kappa opioid receptor (KOR) gene is
constitutively expressed in mouse embryonal carcinoma P19 stem cells
and suppressed by retinoic acid (RA) in cells undergoing neuronal
differentiation. A negative regulatory element is located within intron
1 of the KOR gene, which contains an Ikaros (Ik)-binding
site (GGGAAgGGGAT). This sequence is an Ik-1
respondive, functionally negative element as demonstrated in the
context of both natural KOR and heterologous promoters. The two
underlined G residues of the second half-site are critical for Ik-1
binding and Ik-mediated repression of the KOR gene. RA induces Ik-1
expression within 1 day of treatment and suppresses KOR expression
between 2 and 3 days. Overexpression of Ik-1 in P19 suppresses
endogenous KOR gene expression, accompanied by increased binding of
Ik-1 to the Ik-binding site and chromatin histone deacetylation on KOR
promoters. It is proposed that in an RA-induced P19 differentiation
model, RA elevates Ik-1 expression, which recruits histone
deacetylase to intron 1 of the KOR gene and silences KOR gene promoters.
An Intronic Ikaros-binding Element Mediates Retinoic
Acid Suppression of the Kappa Opioid Receptor Gene, Accompanied
by Histone Deacetylation on the Promoters*
*
This work was supported by National Institutes of
Health Grants DA11190, DA11806, DA70554, and DA00564 (to
H. H. L. and L.-N. W.).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.
To whom correspondence should be addressed: Dept. of Pharmacology,
University of Minnesota Medical School, 6-120 Jackson, 321 Church St.
S. E., Minneapolis, MN 55455. Tel.: 612-625-9402; Fax: 612-625-8408;
E-mail: weixx009@tc.umn.edu.
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