• Bulletin of the Korean Chemical Society
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• v.34 no.1
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• pp.117-120
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• 2013

The reactions of indole with carbonyl groups have been efficiently carried out in the presence of catalytic amounts of 1,3-dibromo-5,5-dimethylhydantoin under solvent-free conditions and corresponding bis(indolyl)-mathanes were obtained in good to excellent yields. Synthesis of di[bis(indolyl)methyl]benzene was also accomplished by this catalyst. Furthermore, chemoselective conversion of aromatic aldehydes to their corresponding bis(indolyl)methanes in the presence of aliphatic aldehydes or ketones was achieved by this method.

• Animal cells and systems
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• v.16 no.2
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• pp.87-94
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• 2012

Nur77 is a member of the nuclear receptor 4A (NR4A) subgroup, which has been implicated in energy metabolism. Although Nur77 is found in adipose tissue, where TR4 plays a key role in lipid homeostasis, the role of Nur77 in adipogenesis is still controversial. Although the Nur77 responsive element (AAAGGTCA) is partially overlapped with TR4-binding sites (AGGTCA $n$ AGGTCA: $n$=0-6), the regulatory role of Nur77 in TR4 function associated with adipocyte biology remains unclear. Here, we found that Nur77 inhibits adipogenesis and TR4 transcriptional activity. Treatment with a Nur77 agonist, 1,1-bis(3'-indolyl)-1-($p$-anisyl)-methane, during 3T3-L1 adipocyte differentiation reduced adipogenesis. In reporter gene analysis, Nur77 specifically suppressed TR4 transcription activity but had little effect on $PPAR{\gamma}$ transcription activity. Consistently, Nur77 also suppressed TR4-induced promoter activity of the TR4 target gene PEPCK, which is known to be important for glyceroneogenesis in adipose tissue. Furthermore, Nur77 suppressed TR4 binding to TR4 response elements without direct interaction with TR4, suggesting that Nur77 may inhibit TR4 transcription activity via binding competition for TR4-binding sites. Furthermore, DIM-C-$pPhOCH_3$ substantially suppressed TR4-induced PEPCK expression in 3T3-L1 adipocytes. Together, our data demonstrate that Nur77 plays an inhibitory role in TR4-induced PEPCK expression in 3T3-L1 adipocytes.