What is the Origin of Glucocorticoid Receptor Action?

The study of steroid hormone receptors, including the GR, is a foundational area of molecular endocrinology, established by the discovery of their nuclear and cytoplasmic localization and function as ligand-activated transcription factors. Understanding GR action is crucial for explaining the systemic effects of cortisol and the therapeutic use of synthetic glucocorticoids. This mechanism underpins the HPA axis feedback loop and its clinical assessment.

What is the Mechanism of Glucocorticoid Receptor Action?

Cortisol diffuses into the target cell and binds to the inactive, cytoplasmic GR complex, causing its conformational change and dissociation from chaperone proteins. The activated GR-cortisol complex then translocates into the nucleus, where it binds to specific DNA sequences called Glucocorticoid Response Elements (GREs) to either activate or repress the transcription of target genes. Furthermore, the GR can exert non-genomic effects and modulate the activity of other transcription factors, such as NF-κB, influencing inflammatory pathways.

Glucocorticoid Receptor Action ∞ Area

Glucocorticoid Receptor Action

Meaning

Glucocorticoid Receptor (GR) action refers to the cellular and molecular events initiated when glucocorticoid hormones, such as cortisol, bind to their specific intracellular receptor protein. This binding event triggers a cascade of effects, primarily altering gene transcription to regulate metabolism, immune response, and inflammation across various tissues. The precise action of the GR is central to the body’s stress response and metabolic homeostasis. This mechanism is critical for the negative feedback control of the HPA axis.