
The glucocorticoid receptor in inflammatory processes : transrepression is not enough
- Author
- Sabine Hübner, Lien Dejager (UGent) , Claude Libert (UGent) and Jan P Tuckermann
- Organization
- Abstract
- Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases. However, steroid therapies are accompanied by severe side-effects during long-term treatment. The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged. Recent discoveries using conditional GR mutant mice and genomic approaches reveal that transactivation of anti-inflammatory acting genes is essential to suppress many inflammatory disease models. This novel view radically changes the concept to design selective acting GR ligands with a reduced side-effect profile.
- Keywords
- inflammation, transactivation, glucocorticoid receptor, ChIP-Seq, transgenic mice, transrepression, INNATE IMMUNE-RESPONSES, INDUCED LEUCINE-ZIPPER, DNA-BINDING, CHROMATIN ACCESSIBILITY, ANTIINFLAMMATORY FUNCTIONS, TRANSCRIPTION FACTORS, TARGET GENES, MAP KINASE, T-CELLS, KAPPA-B
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-6973761
- MLA
- Hübner, Sabine, et al. “The Glucocorticoid Receptor in Inflammatory Processes : Transrepression Is Not Enough.” BIOLOGICAL CHEMISTRY, vol. 396, no. 11, 2015, pp. 1223–31, doi:10.1515/hsz-2015-0106.
- APA
- Hübner, S., Dejager, L., Libert, C., & Tuckermann, J. P. (2015). The glucocorticoid receptor in inflammatory processes : transrepression is not enough. BIOLOGICAL CHEMISTRY, 396(11), 1223–1231. https://doi.org/10.1515/hsz-2015-0106
- Chicago author-date
- Hübner, Sabine, Lien Dejager, Claude Libert, and Jan P Tuckermann. 2015. “The Glucocorticoid Receptor in Inflammatory Processes : Transrepression Is Not Enough.” BIOLOGICAL CHEMISTRY 396 (11): 1223–31. https://doi.org/10.1515/hsz-2015-0106.
- Chicago author-date (all authors)
- Hübner, Sabine, Lien Dejager, Claude Libert, and Jan P Tuckermann. 2015. “The Glucocorticoid Receptor in Inflammatory Processes : Transrepression Is Not Enough.” BIOLOGICAL CHEMISTRY 396 (11): 1223–1231. doi:10.1515/hsz-2015-0106.
- Vancouver
- 1.Hübner S, Dejager L, Libert C, Tuckermann JP. The glucocorticoid receptor in inflammatory processes : transrepression is not enough. BIOLOGICAL CHEMISTRY. 2015;396(11):1223–31.
- IEEE
- [1]S. Hübner, L. Dejager, C. Libert, and J. P. Tuckermann, “The glucocorticoid receptor in inflammatory processes : transrepression is not enough,” BIOLOGICAL CHEMISTRY, vol. 396, no. 11, pp. 1223–1231, 2015.
@article{6973761, abstract = {{Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases. However, steroid therapies are accompanied by severe side-effects during long-term treatment. The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged. Recent discoveries using conditional GR mutant mice and genomic approaches reveal that transactivation of anti-inflammatory acting genes is essential to suppress many inflammatory disease models. This novel view radically changes the concept to design selective acting GR ligands with a reduced side-effect profile.}}, author = {{Hübner, Sabine and Dejager, Lien and Libert, Claude and Tuckermann, Jan P}}, issn = {{1431-6730}}, journal = {{BIOLOGICAL CHEMISTRY}}, keywords = {{inflammation,transactivation,glucocorticoid receptor,ChIP-Seq,transgenic mice,transrepression,INNATE IMMUNE-RESPONSES,INDUCED LEUCINE-ZIPPER,DNA-BINDING,CHROMATIN ACCESSIBILITY,ANTIINFLAMMATORY FUNCTIONS,TRANSCRIPTION FACTORS,TARGET GENES,MAP KINASE,T-CELLS,KAPPA-B}}, language = {{eng}}, number = {{11}}, pages = {{1223--1231}}, title = {{The glucocorticoid receptor in inflammatory processes : transrepression is not enough}}, url = {{http://dx.doi.org/10.1515/hsz-2015-0106}}, volume = {{396}}, year = {{2015}}, }
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