Glucocorticoid Receptor Activation is the process where cortisol or other glucocorticoid hormones bind to their specific intracellular receptors, initiating a cascade of gene transcription events that modulate numerous physiological processes. This activation is central to the body’s stress response, regulating metabolism, immune function, and inflammation. The degree and duration of this activation are clinically significant, as chronic over-activation can lead to catabolism and immune suppression.
Origin
This term is derived from the name of the hormone class, glucocorticoid, and the cellular component, the receptor, which is a protein that binds the hormone. The concept stems from the discovery of steroid hormone action, where the hormone must enter the cell to interact with its nuclear receptor.
Mechanism
Upon cortisol binding, the inactive receptor-hormone complex dissociates from chaperone proteins, translocates into the cell nucleus, and binds to specific DNA sequences called Glucocorticoid Response Elements (GREs). This binding either enhances or represses the transcription of target genes, leading to changes in protein synthesis that govern metabolic shifts, anti-inflammatory effects, and the negative feedback loop that controls HPA axis activity.
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