Review
Oncogene (2006) 25, 6868–6886. doi:10.1038/sj.onc.1209935
Cross-talk between nuclear receptors and nuclear factor 
B
K De Bosscher1, W Vanden Berghe1 and G Haegeman1
1Laboratory for Eukaryotic Gene Expression and Signal Transduction (LEGEST), Department of Molecular Biology, Ghent University, Gent, Belgium
Correspondence: Dr K De Bosscher, Laboratory for Eukaryotic Gene Expression and Signal Transduction, Department of Molecular Biology, Ghent University, KL Ledeganckstraat 35, B-9000 Gent, Belgium. E-mail: karolien.debosscher@ugent.be
Abstract
A variety of studies have shown that some activated nuclear receptors (NRs), especially the glucorticoid receptor, the estrogen receptor and peroxisome proliferator-activated receptor, can inhibit the activity of the transcription factor nuclear factor 
B (NF-B), which plays a key role in the control of genes involved in inflammation, cell proliferation and apoptosis. This review describes the molecular mechanisms of cross-talk between NRs and NF-B and the biological relevance of this cross-talk. The importance and mechanistic aspects of selective NR modulation are discussed. Also included are future research prospects, which will lead to a new era in the field of NR research with the aim of specifically inhibiting NF-B-driven gene expression for anti-inflammatory, anti-tumor and immune-modulatory purposes.
Keywords:
NF-kappaB, hormone, nuclear receptor, glucocorticoid receptor, estrogen receptor, PPAR
Abbreviations:
AP-1, activator protein-1; AR, androgen receptor; Brg1, brahma-related gene 1; BTM, basal transcription machinery; CARM, coactivator-associated arginine methyltransferase; COX, cyclooxygenase; DBD, DNA-binding domain; DRIP, vitamin D receptor-interacting protein; ER, estrogen receptor; FRAP, fluorescence recovery after photobleaching; GILZ, glucocorticoid-induced leucine zipper; GR, glucocorticoid receptor; GRIP, glucocorticoid receptor-interacting protein; (n)GRE, (negative) glucocorticoid response element; HAT, histone acetyltransferase; HDAC, histone deacetylase; Hsp, heat shock protein; IB, inhibitor B; IKK, IB kinase; IL, interleukin; iNOS, inducible nitric oxide synthase; LBD, ligand-binding domain; LSD1, lysine-specific histone demethylase 1; LXR, liver X receptor; MAPK, mitogen-actived protein kinase; MKP-1, mitogen-activated protein kinase phosphatase 1; MMP, matrix metalloproteinase; MR, mineralocorticoid receptor; MTA, metastasis-associated protein; NcoR, nuclear corepressor; NF-B, nuclear factor B; NR, nuclear receptor; PGC-1, PPAR
coactivator-1; PPAR, peroxisome proliferator-activated receptor; PK, protein kinase; PLA, phospholipase A; PR, progesterone receptor; PSA, prostate-specific antigen; p-TEFb, transcription elongation factor; pol, polymerase; RAR/RXR, retinoid acid receptor/retinoid X receptor; SEGRM, selective GR modulators; SERM, selective ER modulators; SMRT, silencing mediator of retinoic-acid and thyroid hormone receptors; SRC-1, steroid receptor coactivator-1; TBL1, transducin-
-like 1; TF, transcription factor; TIF, transcription intermediary factor; TLR, toll-like receptor; TNF, tumor necrosis factor; TR, thyroid hormone receptor; TRAP, thyroid receptor-activated protein
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