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Biotin analogs activate guanylate cyclase.

D L Vesely, H C Wormser, H N Abramson

    Molecular and Cellular Biochemistry
    |January 1, 1984
    PubMed
    Summary

    Biotin analogs lacking sulfur significantly enhance guanylate cyclase activity, challenging the sulfur atom's essential role. This suggests structural components beyond sulfur are key to biotin's function in enzyme activation.

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    Area of Science:

    • Biochemistry
    • Enzymology
    • Molecular Biology

    Background:

    • The role of the sulfur atom in vitamin biotin's biological activity has been a subject of prior investigation.
    • Biotin has recently been identified as an activator of guanylate cyclase, an important enzyme.

    Purpose of the Study:

    • To investigate the structure-function relationship of biotin concerning its mechanism of action.
    • To determine if the sulfur atom is essential for biotin's ability to activate guanylate cyclase.

    Main Methods:

    • Synthesized and tested biotin analogs (azabiotin, bisnorazabiotin, carbobiotin, isoazabiotin) lacking a sulfur atom.
    • Assessed the effect of these analogs on guanylate cyclase activity in various tissues (liver, cerebellum, heart, kidney, colon).
    • Determined the effective dose (ED50) for guanylate cyclase stimulation by the analogs.

    Main Results:

    • Biotin analogs without sulfur significantly enhanced guanylate cyclase activity (two-fold increase at 1 microM).
    • The ED50 for guanylate cyclase stimulation by these analogs was 0.1 microM.
    • Even a simple 5-membered ring compound (2-imidazolidone) showed guanylate cyclase augmenting activity.
    • Manganese cofactor was not essential for initial enhancement but was required for maximal activation.

    Conclusions:

    • The sulfur atom is not essential for biotin's activation of guanylate cyclase.
    • The structural components of biotin, particularly the ring system, are crucial for guanylate cyclase activation.
    • Further research into biotin analogs can elucidate enzyme activation mechanisms.

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