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ACTH antagonists.

K Hofmann, J A Montibeller, F M Finn

    Proceedings of the National Academy of Sciences of the United States of America
    |January 1, 1974
    PubMed
    Summary
    This summary is machine-generated.

    Structural modifications of adrenocorticotropic hormone (ACTH) analogs reveal tryptophan

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    Area of Science:

    • Biochemistry
    • Endocrinology
    • Molecular Pharmacology

    Background:

    • Adrenocorticotropic hormone (ACTH) regulates adrenal cortical function via adenylate cyclase.
    • The precise molecular interactions of ACTH with its receptor and downstream signaling remain incompletely understood.
    • Identifying key residues for ACTH's biological activity is crucial for developing targeted therapeutics.

    Purpose of the Study:

    • To investigate the role of specific amino acid residues in ACTH's interaction with the adenylate cyclase system.
    • To synthesize and characterize ACTH analogs with modified active sites.
    • To determine the relationship between receptor binding affinity and adenylate cyclase activation.

    Main Methods:

    • Synthesis of modified ACTH analogs, including [Gln(5), Phe(9)]corticotropin(1-20) amide and [N(alpha)-Metrp(9)]corticotropin(1-24).

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  • Assay of adenylate cyclase activity in bovine adrenal cortical plasma membranes.
  • Evaluation of ACTH analog binding affinity to ACTH receptors.
  • Comparison of hormonal and fluoride-ion-mediated adenylate cyclase activation.

    • Main Results:

    • The tryptophan residue in ACTH is essential for stimulating adenylate cyclase.
    • Modified ACTH analogs ([Gln(5), Phe(9)]corticotropin(1-20) amide, [N(alpha)-Metrp(9)]corticotropin(1-24)) exhibit high receptor affinity but lack cyclase activity.
    • Fluoride-activated adenylate cyclase is not inhibited by these ACTH antagonists, suggesting distinct activation pathways.

    Conclusions:

    • Receptor affinity alone is insufficient for eliciting a hormonal response.
    • The tryptophan residue is critical for the signaling function of ACTH.
    • Hormonal and fluoride-induced activation of adenylate cyclase involve different mechanisms.