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Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatases

Ilse Beck UGent, Wim Vanden Berghe UGent, Linda Vermeulen UGent, Keith R Yamamoto, Guy Haegeman UGent and Karolien De Bosscher UGent (2009) ENDOCRINE REVIEWS. 30(7). p.830-882
abstract
Glucocorticoids (GCs) are steroidal ligands for the GC receptor (GR), which can function as a ligand-activated transcription factor. These steroidal ligands and derivatives thereof are the first line of treatment in a vast array of inflammatory diseases. However, due to the general surge of side effects associated with long-term use of GCs and the potential problem of GC resistance in some patients, the scientific world continues to search for a better understanding of the GC-mediated antiinflammatory mechanisms. The reversible phosphomodification of various mediators in the inflammatory process plays a key role in modulating and fine-tuning the sensitivity, longevity, and intensity of the inflammatory response. As such, the antiinflammatory GCs can modulate the activity and/or expression of various kinases and phosphatases, thus affecting the signaling efficacy toward the propagation of proinflammatory gene expression and proinflammatory gene mRNA stability. Conversely, phosphorylation of GR can affect GR ligand- and DNA-binding affinity, mobility, and cofactor recruitment, culminating in altered transactivation and transrepression capabilities of GR, and consequently leading to a modified antiinflammatory potential. Recently, new roles for kinases and phosphatases have been described in GR-based antiinflammatory mechanisms. Moreover, kinase inhibitors have become increasingly important as antiinflammatory tools, not only for research but also for therapeutic purposes. In light of these developments, we aim to illuminate the integrated interplay between GR signaling and its correlating kinases and phosphatases in the context of the clinically important combat of inflammation, giving attention to implications on GC-mediated side effects and therapy resistance.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
EPITHELIAL NA+ CHANNEL, TUMOR-NECROSIS-FACTOR, DUAL-SPECIFICITY PHOSPHATASE-1, TOLL-LIKE RECEPTOR, DNA-BINDING DOMAIN, ACTIVATED PROTEIN-KINASE, INDUCED LEUCINE-ZIPPER, NF-KAPPA-B, INNATE IMMUNE-RESPONSES, SIGNAL-REGULATED KINASE
journal title
ENDOCRINE REVIEWS
Endocr. Rev.
volume
30
issue
7
pages
830 - 882
Web of Science type
Review
Web of Science id
000272472800003
JCR category
ENDOCRINOLOGY & METABOLISM
JCR impact factor
19.761 (2009)
JCR rank
1/104 (2009)
JCR quartile
1 (2009)
ISSN
0163-769X
DOI
10.1210/er.2009-0013
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
955766
handle
http://hdl.handle.net/1854/LU-955766
date created
2010-05-27 11:32:15
date last changed
2010-07-16 12:20:13
@article{955766,
  abstract     = {Glucocorticoids (GCs) are steroidal ligands for the GC receptor (GR), which can function as a ligand-activated transcription factor. These steroidal ligands and derivatives thereof are the first line of treatment in a vast array of inflammatory diseases. However, due to the general surge of side effects associated with long-term use of GCs and the potential problem of GC resistance in some patients, the scientific world continues to search for a better understanding of the GC-mediated antiinflammatory mechanisms. The reversible phosphomodification of various mediators in the inflammatory process plays a key role in modulating and fine-tuning the sensitivity, longevity, and intensity of the inflammatory response. As such, the antiinflammatory GCs can modulate the activity and/or expression of various kinases and phosphatases, thus affecting the signaling efficacy toward the propagation of proinflammatory gene expression and proinflammatory gene mRNA stability. Conversely, phosphorylation of GR can affect GR ligand- and DNA-binding affinity, mobility, and cofactor recruitment, culminating in altered transactivation and transrepression capabilities of GR, and consequently leading to a modified antiinflammatory potential. Recently, new roles for kinases and phosphatases have been described in GR-based antiinflammatory mechanisms. Moreover, kinase inhibitors have become increasingly important as antiinflammatory tools, not only for research but also for therapeutic purposes. In light of these developments, we aim to illuminate the integrated interplay between GR signaling and its correlating kinases and phosphatases in the context of the clinically important combat of inflammation, giving attention to implications on GC-mediated side effects and therapy resistance.},
  author       = {Beck, Ilse and Vanden Berghe, Wim and Vermeulen, Linda and Yamamoto, Keith R and Haegeman, Guy and De Bosscher, Karolien},
  issn         = {0163-769X},
  journal      = {ENDOCRINE REVIEWS},
  keyword      = {EPITHELIAL NA+ CHANNEL,TUMOR-NECROSIS-FACTOR,DUAL-SPECIFICITY PHOSPHATASE-1,TOLL-LIKE RECEPTOR,DNA-BINDING DOMAIN,ACTIVATED PROTEIN-KINASE,INDUCED LEUCINE-ZIPPER,NF-KAPPA-B,INNATE IMMUNE-RESPONSES,SIGNAL-REGULATED KINASE},
  language     = {eng},
  number       = {7},
  pages        = {830--882},
  title        = {Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatases},
  url          = {http://dx.doi.org/10.1210/er.2009-0013},
  volume       = {30},
  year         = {2009},
}

Chicago
Beck, Ilse, Wim Vanden Berghe, Linda Vermeulen, Keith R Yamamoto, Guy Haegeman, and Karolien De Bosscher. 2009. “Crosstalk in Inflammation: The Interplay of Glucocorticoid Receptor-based Mechanisms and Kinases and Phosphatases.” Endocrine Reviews 30 (7): 830–882.
APA
Beck, I., Vanden Berghe, W., Vermeulen, L., Yamamoto, K. R., Haegeman, G., & De Bosscher, K. (2009). Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatases. ENDOCRINE REVIEWS, 30(7), 830–882.
Vancouver
1.
Beck I, Vanden Berghe W, Vermeulen L, Yamamoto KR, Haegeman G, De Bosscher K. Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatases. ENDOCRINE REVIEWS. 2009;30(7):830–82.
MLA
Beck, Ilse, Wim Vanden Berghe, Linda Vermeulen, et al. “Crosstalk in Inflammation: The Interplay of Glucocorticoid Receptor-based Mechanisms and Kinases and Phosphatases.” ENDOCRINE REVIEWS 30.7 (2009): 830–882. Print.