What characteristic of the glucocorticoid receptor contributes to the lasting effects of dexamethasone even after it's eliminated from the body?

The lasting effects of dexamethasone, a synthetic glucocorticoid, can largely be attributed to its ability to induce the expression of specific proteins that continue to exert their effects even after the drug has been cleared from the body. Glucocorticoids, upon binding to their receptor, enter the cell nucleus and function as transcription factors, leading to the upregulation or downregulation of various target genes.

Once dexamethasone binds to the glucocorticoid receptor, this complex can promote the synthesis of proteins that may have prolonged biological activity. These proteins often play roles in mediating anti-inflammatory effects, stress responses, and other metabolic functions. As a result, even after dexamethasone is eliminated from circulation, the proteins it induced can persist and continue to modify physiological responses, thereby prolonging its effects.

The other options do not accurately capture this mechanism. For instance, the ability to catalyze formation of tyrosine-phosphate bonds is more relevant to receptor tyrosine kinases rather than glucocorticoid receptors. Competing with β-arrestin relates to the modulation of receptor signaling pathways, but it does not explain the duration of effects post-elimination. Deple