The measure of how accurately and effectively the signal initiated by the testosterone hormone is transmitted from the androgen receptor (AR) on the cell surface or within the cytoplasm to the target DNA in the nucleus. High fidelity implies a robust, correct, and timely downstream gene expression response, whereas low fidelity can result from genetic variants in the AR or impaired co-factor availability, leading to suboptimal biological effects despite adequate circulating hormone levels. Maintaining this fidelity is essential for full hormonal efficacy.
Origin
This concept merges the specific hormone and its pathway, Testosterone Signaling, with the engineering term Fidelity, which denotes the degree of exactness with which something is copied or reproduced. It is a key concept in andrology and molecular endocrinology, focusing on the quality, not just the quantity, of the hormonal message.
Mechanism
The process begins with testosterone binding to the androgen receptor (AR), which then translocates to the nucleus and binds to specific DNA sequences known as Androgen Response Elements (AREs). Fidelity can be compromised by genetic polymorphisms in the AR gene, such as variations in the CAG repeat length, which affect the receptor’s transcriptional activity. The mechanism of maintaining fidelity involves ensuring optimal receptor structure and the presence of necessary co-activator proteins for precise gene transcription.
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