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. 2022 Dec 27;59(1):56. doi: 10.3390/medicina59010056

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Genomic mechanisms of glucocorticoid-induced anti-inflammation. GCs bind to their cytosolic glucocorticoid receptor (GCR), which subsequently loses its chaperoning proteins, such as heat shock proteins (Hsp). Homodimers are formed, travel to the nucleus, bind to the glucocorticoid response element (GRE), and upregulate the expression of certain genes (e.g., lipocortin-1 and genes involved in metabolism), a mechanism called transactivation. Monomeric GC–GCR complex (mGC-GCR) can bind to transcription factors as AP-1 and NF-kβ, inhibiting the transcription of their target genes (e.g., IL-2 and TNFα) by a mechanism called transrepression. Further, direct binding of mGC-GCR alongside AP-1 on composite GREs lead to transrepression. Created with BioRender.com (accessed on 17 October 2022).