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¹ Department of Dental and Medical Biochemistry, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan
² Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan
³ Department of Biochemistry, Nihon University School of Medicine, Tokyo 173-8610, Japan

DEC1 (BHLHB2/Stra13/Sharp2)—a basic helix-loop-helix transcription factor—is known to be involved in various biological phenomena including clock systems and metabolism. In the clock systems, Dec1 expression is dominantly up-regulated by CLOCK : BMAL1 heterodimer, and it exhibits circadian rhythm in the suprachiasmatic nucleus (SCN)—the central circadian pacemaker—and other peripheral tissues. Recent studies have shown that the strong circadian rhythmicity of Dec1 in the SCN was abolished by Clock mutation, whereas that in the liver was affected, but not abolished, by Clock mutation. Moreover, feeding conditions affected hepatic Dec1 expression, which indicates that Dec1 expression is closely linked with the metabolic functions of the liver. Among ligand-activated nuclear receptors examined, LXR and LXRβ with T0901317—agonist for LXR—were found to be potent enhancers for Dec1 promoter activity, and a higher expression level of LXR protein was detected in the liver than in the kidney and heart. T0901317 increased the levels of endogenous Dec1 transcript in hepatoma cells. Chromatin immunoprecipitation assay indicated that LXR bound to the Dec1 promoter, and an LXR-binding site was identified. These observations indicate that hepatic DEC1 mediates the ligand-dependent LXR signal to regulate the expression of genes involved in the hepatic clock system and metabolism.

^* Correspondence: noshiro{at}hiroshima-u.ac.jp

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