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Related Experiment Videos

Calcium, phospholipid turnover and transmembrane signalling.

Y Nishizuka

    Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
    |July 5, 1983
    PubMed
    Summary

    Phosphatidylinositol turnover signals protein phosphorylation via C-kinase activation, requiring calcium (Ca2+) and phosphatidylserine. Full cellular response needs both receptor signaling and Ca2+ mobilization synergistically.

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    Area of Science:

    • Cellular signaling pathways
    • Biochemistry
    • Molecular biology

    Background:

    • Phosphatidylinositol turnover is triggered by various biological substances.
    • This turnover is linked to transmembrane control of protein phosphorylation.
    • A novel protein kinase, C-kinase, is involved in this process.

    Purpose of the Study:

    • To investigate the role of phosphatidylinositol turnover in cellular signaling.
    • To elucidate the activation mechanism of C-kinase.
    • To determine the synergistic requirements for a full cellular response.

    Main Methods:

    • Utilized synthetic diacylglycerol to activate C-kinase directly.
    • Employed the Ca2+ ionophore A23187 for calcium mobilization.
    • Investigated the effects of cyclic nucleotides (cAMP, cGMP) on phosphatidylinositol breakdown.

    Main Results:

    • C-kinase activation requires calcium (Ca2+) and phosphatidylserine.
    • Diacylglycerol enhances C-kinase affinity for Ca2+, leading to full activation without increased Ca2+ levels.
    • Both receptor-linked protein phosphorylation and Ca2+ mobilization are synergistically required for a complete cellular response.
    • Cyclic nucleotides can inhibit phosphatidylinositol breakdown, providing negative feedback.

    Conclusions:

    • Phosphatidylinositol turnover acts as a crucial signal for C-kinase mediated protein phosphorylation.
    • Synergistic action of receptor signaling and calcium is essential for cellular activation.
    • Cyclic nucleotides play a regulatory role in preventing cellular over-response.

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