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M210486200v1
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Papers In Press, published online ahead of print February 28, 2003
J. Biol. Chem, 10.1074/jbc.M210486200
Submitted on October 13, 2002
Revised on February 28, 2003
Accepted on February 28, 2003

Upstream stimulatory factor represses the induction of carnitine palmitoyltransferase-Ibeta expression by PGC-1

Meredith L. Moore, Edwards A. Park, and Jeanie B. McMillin

Pathology and Laboratory Medicine, University of Texas Medical School at Houston, Houston, TX 77030

Corresponding Author: Jeanie.B.McMillin{at}uth.tmc.edu

Transcriptional regulation of carnitine palmitoyltransferase-1b (CPT-1b) is coordinated with contractile gene expression through the cardiac-enriched transcription factors, GATA4 and SRF. Metabolic modulation of CPT-1b promoter activity has been described with the stimulation of gene expression by oleate that is mediated through the peroxisome proliferator activated receptor (PPAR) pathway. The coactivator, peroxisomal proliferator activated receptor g coactivator (PGC-1), enhances gene expression through interactions with nuclear hormone receptors and the myocyte enhancer factor 2 (MEF2) family. PGC-1 and MEF2A synergistically activate CPT-1b promoter activity. This stimulation is enhanced by mutation of the E-box sequences that flank the MEF2A binding site. These elements bind the Upstream Stimulatory Factors (USF1 and USF2), which activate transcription in CV-1 fibroblasts. However, overexpression of the USF proteins in myocytes depresses CPT-1b activity and significantly reduces MEF2A and PGC-1 synergy. Co-immunoprecipitation studies demonstrate that PGC-1 and USF2 proteins can physically interact. Our studies demonstrate that PGC-1 stimulates CPT-1b gene expression through MEF2A. USF proteins have a novel role in repressing the expression of the CPT-1b gene and modulating the induction by the coactivator, PGC-1.


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