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J. Biol. Chem., Vol. 278, Issue 28, 25281-25284, July 11, 2003
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ACCELERATED PUBLICATIONS
(PPAR)-interacting Protein, Is Required for PPAR-mediated Adipogenesis*
From the Department of Pathology, Northwestern University, The Feinberg School of Medicine, Chicago, Illinois 60611-3008
Nuclear receptor coactivator PRIP (peroxisome proliferators-activated
receptor (PPAR
)-interacting protein) appears to serve as a linker
between cAMP response element-binding protein-binding protein
(CBP/p300)anchored and PBP (PPAR-binding protein)-anchored coactivator
complexes involved in the transcriptional activity of nuclear receptors.
Disruption of PRIP and PBP genes results in embryonic lethality between
embryonic day 11.5 and 12.5 (postcoitum), indicating that PRIP and PBP are
essential and nonredundant coactivators. Both PRIP and PBP were initially
identified as PPAR coactivators, suggesting a role for these molecules
in PPAR-induced adipogenesis.
PBP–/– mouse embryonic
fibroblasts fail to exhibit PPAR-stimulated adipogenesis indicating
that PBP is a downstream regulator of PPAR-mediated adipogenesis. We
now show that PRIP–/– mouse
embryonic fibroblasts are also refractory to PPAR-stimulated
adipogenesis and fail to express adipogenic marker aP2, a
PPAR-responsive gene. Chromatin immunoprecipitation assays reveal
reduced association in PRIP–/–
cells of PIMT (PRIP-binding protein) and PBP with aP2 gene promoter,
suggesting that PRIP is required for the linking of CBP/p300-anchored cofactor
complex with PBP-anchored mediator complex. These data indicate that PRIP,
like PBP, is a downstream regulator of PPAR-mediated adipogenesis and
that both these coactivators are required for the successful completion of
adipogenic program.
Received for publication, April 23, 2003
* This work was supported by National Institutes of Health Grants GM23750 (to J. K. R.), CA84472 (to M. S. R.), and CA64239 and K08 ES00356 (to Y.-J. Z.) and by the Joseph L. Mayberry Sr. Endowment Fund. The costs of publication of this article were defrayed in part by the payment of page charges. This 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 Pathology, Northwestern
University, Feinberg School of Medicine, 303 East Chicago Ave., Chicago, IL
60611-3008. Tel.: 312-503-8144; Fax: 312-503-8249; E-mail:
jkreddy{at}northwestern.edu.
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