A comprehensive analysis of the glucocorticoid-sensitive pro-inflammatory genes in macrophages reveals fundamental differences between the temporal events and components of transcriptional machinery that the glucocorticoid receptor targets to repress their transcription.

A human experimental model for physiological glucocorticoid exposure and glucocorticoid withdrawal identifies a multi-omic cluster, including microRNA miR-122-5p and metabolites, associated with glucocorticoid-responsive genes.

Although developing oocytes and sperm of mice both harbor the glucocorticoid receptor, fetal oocytes are resistant to differing levels of gluocorcorticoid stress hormones, while spermatogonia alter RNA splicing.

Within distinct chromatin landscapes, the BRG1 chromatin remodeling enzyme patterns hormone-dependent chromatin interactions, pioneer factor recruitment, and transcriptional activity.

Hepatic TAZ coordinates the differential expression of gluconeogenic genes in the fasted and fed states by inhibiting glucocorticoid receptor.

Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

Epigenetic regulation of the glucocorticoid receptor in castration-resistant prostate cancer can be targeted via the use of BET bromodomain inhibitors.

Deletion of β-catenin in Col2⁺ progenitor cells shifts their commitment from osteoblasts to adipocytes, leading to a full spectrum of disease phenotype of glucocorticoid-induced osteonecrosis of the femoral head in adult mice.

Behavioral analyses and an optogenetic approach reveal an existence of GR-mediated metaplasticity in the LA and its link with adaptive fear response to auditory cues in a stressful condition.

LDT-VTA dysfunction induced by prenatal glucocorticoid exposure leads to reward deficits that can be ameliorated by selective optogenetic activation of this circuit.