Transactivation<unk> s bind to the cytosolic<unk>  receptor, a type of nuclear receptor that is activated by ligand binding. After a hormone binds to the corresponding receptor, the newly formed complex translocates itself into the cell nucleus, where it binds to<unk>  response elements in the promoter region of the target genes resulting in the regulation of gene expression. This process is commonly referred to as transcriptional activation, or transactivation. The proteins encoded by these up-regulated genes have a wide range of effects, including, for example: * anti-inflammatory – lipocortin I, p11/calpactin binding protein, secretory leukocyte protease inhibitor 1 (SLPI), and Mitogen-activated protein kinase phosphatase (MAPK phosphatase) * increased gluconeogenesis – glucose 6-phosphatase and tyrosine aminotransferase Transrepression The opposite mechanism is called transcriptional repression, or transrepression. The classical understanding of this mechanism is that activated<unk>  receptor binds to DNA in the same site where another transcription factor would bind, which prevents the transcription of genes that are transcribed via the activity of that factor. While this does occur, the results are not consistent for all cell types and conditions; there is no generally accepted, general mechanism for transrepression. New mechanisms are being discovered where transcription is repressed, but the activated<unk>  receptor is not interacting with DNA, but rather with another transcription factor directly, thus interfering with it, or with other proteins that interfere with the function of other transcription factors. This latter mechanism appears to be the most likely way that activated<unk>  receptor interferes with NF-κB - namely by recruiting histone deacetylase, which deacetylate the DNA in the promoter region leading to closing of the chromatin structure where NF-κB needs to bind. Nongenomic effects Activated<unk>  receptor has effects that have been experimentally shown to be independent of any effects on transcription and can only be due to direct binding of activated<unk>  receptor with other proteins or with mRNA. For example, Src kinase which binds to inactive<unk>  receptor, is released when a<unk>  binds to<unk>  receptor, and phosphorylates a protein that in turn displaces an adaptor protein from a receptor important in inflammation, epidermal growth factor, reducing its activity, which in turn results in reduced creation of arachidonic acid - a key proinflammatory molecule. This is one mechanism by which<unk> s have an anti-inflammatory effect.
Glucocorticoid
Adrenal steroid
Corticosteroid
Antiglucocorticoid
Xenohormone
Anticorticotropin
Phytosteroid
Neurohormone