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Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era by Anthony N. Gerber; Robert Newton; Sarah K. Sasse is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Glucocorticoids are potent anti-inflammatory drugs that are used to treat an extraordinary range of human disease, including COVID-19, underscoring the ongoing importance of understanding their molecular mechanisms. Early studies of GR signaling led to broad acceptance of models in which glucocorticoid receptor (GR) monomers tether repressively to inflammatory transcription factors, thus abrogating inflammatory gene expression. However, newer data challenge this core concept and present an exciting opportunity to reframe our understanding of GR signaling. Here, we present an alternate, two-part model for transcriptional repression by glucocorticoids. First, widespread GR-mediated induction of transcription results in rapid, primary repression of inflammatory gene transcription and associated enhancers through competition-based mechanisms. Second, a subset of GR-induced genes, including targets that are regulated in coordination with inflammatory transcription factors such as NF-κB, exerts secondary repressive effects on inflammatory gene expression. Within this framework, emerging data indicate that the gene set regulated through the cooperative convergence of GR and NF-κB signalin

Who reads Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era?

Author

Anthony N. Gerber; Robert Newton; Sarah K. Sasse

Publisher

Elsevier BV

Published

2021

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)