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Strickland, B.A.* ; Ansari, S.A. ; Dantoft, W. ; Uhlenhaut, N.H.

How to tame your genes: Mechanisms of inflammatory gene repression by glucocorticoids.

FEBS Lett. 596, 2596-2616 (2022)
Verlagsversion DOI PMC
Open Access Hybrid
Glucocorticoids (GCs) are widely used therapeutic agents to treat a broad range of inflammatory conditions. Their functional effects are elicited by binding to the glucocorticoid receptor (GR), which regulates transcription of distinct gene networks in response to ligand. However, the mechanisms governing various aspects of undesired side effects versus beneficial immunomodulation upon GR activation remain complex and incompletely understood. In this review, we discuss emerging models of inflammatory gene regulation by GR, highlighting GR's regulatory specificity conferred by context-dependent changes in chromatin architecture and transcription factor or co-regulator dynamics. GR controls both gene activation and repression, with the repression mechanism being central to favourable clinical outcomes. We describe current knowledge about 3D genome organisation and its role in spatiotemporal transcriptional control by GR. Looking beyond, we summarise the evidence for dynamics in gene regulation by GR through cooperative convergence of epigenetic modifications, transcription factor crosstalk, molecular condensate formation and chromatin looping. Further characterising these genomic events will reframe our understanding of mechanisms of transcriptional repression by GR.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Chromatin ; Epigenetic ; Gene Repression ; Glucocorticoid ; Glucocorticoid Receptor ; Inflammation ; Macrophage ; Phase Condensates ; Transcription
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 0014-5793
e-ISSN 1873-3468
Zeitschrift FEBS Letters
Quellenangaben Band: 596, Heft: 20, Seiten: 2596-2616 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-227
G-502595-001
Förderungen Else Kroner-Fresenius-Stiftung
Deutsche Forschungsgemeinschaft
DOI 10.1002/1873-3468.14409
WOS ID WOS:000810262000001
PubMed ID 35612756
Erfassungsdatum 2022-06-28
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