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Triphenylethylene antiestrogen binding sites (TABS) specificity.

J H Clark, W C Mitchell, S C Guthrie

    Journal of Steroid Biochemistry
    |April 1, 1987
    PubMed
    Summary
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    This study investigated triphenylethylene antiestrogen binding sites (TABS) and found their affinity for various compounds, including cholesterol, suggests roles beyond estrogen antagonism, possibly in calmodulin function or cholesterol metabolism.

    Area of Science:

    • Biochemistry
    • Molecular Pharmacology
    • Endocrinology

    Background:

    • Triphenylethylene antiestrogens are known to interact with specific binding sites.
    • The precise function of these antiestrogen binding sites (TABS) remains unclear.
    • Understanding TABS interactions is crucial for developing targeted therapies.

    Purpose of the Study:

    • To determine the relative binding affinities (RBA) of various compounds to TABS.
    • To elucidate the potential roles of TABS based on their binding profiles.
    • To compare the binding of triphenylethylenes with other classes of molecules.

    Main Methods:

    • Competitive binding assays using [3H]tamoxifen as a tracer.
    • Extraction of TABS from rat liver nuclei.

    Related Experiment Videos

  • Quantification of relative binding affinities (RBA) and dissociation constants (Kd).

    • Main Results:

    • Nafoxidine exhibited the highest RBA (333) for TABS, with a Kd of approximately 0.3 nM.
    • Tamoxifen, zuclomiphene, and enclomiphene showed comparable RBAs.
    • Trifluoperazine and cholesterol derivatives demonstrated significant binding affinities, suggesting potential links to calmodulin and cholesterol metabolism.

    Conclusions:

    • TABS are unlikely to be directly involved in estrogen antagonism due to divergent activities of triphenylethylenes.
    • The observed binding of trifluoperazine suggests a potential role for TABS in calmodulin regulation.
    • Significant binding of cholesterol and 7-ketocholesterol indicates TABS may be involved in cholesterol metabolism.