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lüll Control of gene expression by glucocorticoid hormones Rousseau GGBiochem J 1984[Nov]; 224 (1): 1-12Glucocorticoids control the expression of a small number of transcriptionally active genes by increasing or decreasing mRNA concentration. Either effect can result from a transcriptional or a post-transcriptional mechanism. Induction of mouse mammary tumour virus RNA results from a stimulation of transcription initiation and depends on the presence of defined regions in proviral DNA. These regions bind the glucocorticoid receptor and behave functionally as proto-enhancers. Glucocorticoid-inducible genes can retain their sensitivity to the hormone after transfer to a heterologous cell by transfection techniques. Non-inducible genes can become inducible when linked to the promoter region of an inducible gene. The mechanisms by which the receptor-steroid complex stimulates or inhibits transcription or influences mRNA stability are unknown. Receptor binding to nucleic acids appears to be a necessary but not sufficient condition. It is likely that the receptor also interacts with chromatin proteins. This might lead to a catalytic modification of these proteins, resulting in a modulation of gene expression. Development of glucocorticoid-sensitive, biochemically defined, cell-free transcription systems should provide a tool to delineate the molecular determinants of this essential regulatory mechanism.|Animals[MESH]|Chromatin/drug effects/metabolism[MESH]|DNA/genetics/metabolism[MESH]|Gene Expression Regulation/*drug effects[MESH]|Genes/drug effects[MESH]|Glucocorticoids/pharmacology/*physiology[MESH]|Humans[MESH]|Mammary Tumor Virus, Mouse/genetics[MESH]|Mice[MESH]|Models, Genetic[MESH]|RNA, Messenger/metabolism[MESH]|Rats[MESH]|Receptors, Glucocorticoid/metabolism[MESH]|Transcription, Genetic/drug effects[MESH]|Transfection[MESH] |