Biochemical and Biophysical Research Communications
Regular ArticleGM-CSF Expression in Pulmonary Epithelial Cells Is Regulated Negatively by Posttranscriptional Mechanisms
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2019, Pharmacology and TherapeuticsCitation Excerpt :In transactivation, glucocorticoid-bound GR binds to GREs present in DNA, enhancing associated gene expression (Newton, 2014; Vandevyver et al., 2013). Many of the genes induced have anti-inflammatory activity and contribute to the significant post-transcriptional repression of inflammatory protein production mediated with glucocorticoid treatment (Fan et al., 2006; Ing, 2005; Newton, 2014; Newton, Staples, Hart, Barnes, & Bergmann, 2001). ICS-inducible genes also repress inflammatory pathways, with cyclin-dependent kinase inhibitor 1C (CDKN1C) and dual specificity protein phosphatase 1 (DUSP1/MKP1) suppressing inflammatory mitogen-activated protein kinase (MAPK) pathways, while TSC22 domain family protein 3 (TSC22D3/GILZ) attenuates NF-κB and AP-1 activity (Ayroldi & Riccardi, 2009; Chang et al., 2003; King, Holden, Gong, Rider, & Newton, 2009; Mittelstadt & Ashwell, 2001; Newton, 2014).
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2004, Journal of Biological ChemistryCitation Excerpt :Thus in many cases steady state mRNA levels were either unaffected or were potentiated. A similar effect was reported in respect of GM-CSF, expression of which was markedly increased by D609 via a mechanism that was at least partly due to a profound mRNA stabilization (63). This phenomenon, coupled with the global changes in histone acetylation observed following D609 treatment, have led us to treat these data with caution.
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