Intracellular Receptor Binding describes the specific molecular interaction where a signaling molecule, typically a lipophilic ligand such as a steroid hormone, passes through the plasma membrane to physically associate with its cognate receptor located within the cell’s cytoplasm or nucleus. This binding event is the critical first step in initiating the genomic effects of many vital hormones. Without successful binding, the hormonal signal cannot be transduced into a nuclear action to alter gene transcription. This step confirms the cell’s responsiveness to the circulating signal.
Origin
The mechanism is central to the action of steroid and thyroid hormones, established through research differentiating them from peptide hormones that bind to surface receptors. The term merges ‘intracellular’ (within the cell) with ‘receptor binding’ (ligand-protein interaction). Its origin in endocrinology clarified why these hormones exhibit prolonged effects, as they directly influence the cellular machinery for protein synthesis. Understanding this location of action is key to understanding hormone pharmacology.
Mechanism
Upon binding the ligand, the receptor typically undergoes a conformational change, often exposing a DNA-binding domain which allows the activated complex to translocate to the nucleus if necessary and bind to specific hormone response elements on the chromatin. This binding event recruits coactivator proteins, initiating the transcription of target genes responsible for the cell’s ultimate physiological response. The strength and duration of this binding event directly correlate with the magnitude of the subsequent physiological effect.
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