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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: Steroids. 2017 Nov 10;133:60–66. doi: 10.1016/j.steroids.2017.11.002

Figure 1.

Figure 1

Glucocorticoid receptor (GR) regulation and signaling. (A) Schematic representation of regulation of glucocorticoid (GC) levels by the hypothalamic-pituitary adrenal (HPA) axis, and the regulation of the conversion between the biologically active form of GCs, cortisol and the inactive form, cortisone, by 11β-hydroxysteroid dehydrogenase type 1 and type 2. (B) Representation of GR structure containing N-terminal transactivation domain (NTD), a central DNA binding domain (DBD), a flexible hinge region (H) and a C-terminal ligand binding domain (LBD). (C) GR isoforms generated by alternative splicing. (D) GR signaling following the binding of GCs to the cytoplasmic GR, which then undergoes conformational changes that result in the dissociation from accessory proteins and translocation to the nucleus. In the nucleus, GR regulates the expression of target genes by multiple ways such as a direct binding to glucocorticoid-response elements (GRE) and activation of glucocorticoid-induced leucine zipper (GILZ) transcription factor.