What question did this study set out to answer?

To determine whether protein kinase C regulates thrombin-induced inositol trisphosphate formation and activation responses in human platelets using kinase inhibitors.

January 15, 1988Biochemical JournalOpen Access

The action of the protein kinase C inhibitor, staurosporine, on human platelets. Evidence against a regulatory role for protein kinase C in the formation of inositol trisphosphate by thrombin

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Authors

SWSteve P. WatsonVascular Medicine JMJ McNallyCzech Academy of Sciences LSLorna J. ShipmanUniversity of Oxford

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Implication

In vitro study demonstrates staurosporine inhibits secretion without altering inositol phosphate levels in human platelets, indicating protein kinase C does not regulate phosphoinositide metabolism.

Key Points

To determine whether protein kinase C regulates thrombin-induced inositol trisphosphate formation and activation responses in human platelets using kinase inhibitors.
Assessed putative protein kinase C inhibitors (staurosporine, polymyxin B, C-1, H-7, tamoxifen) on dioctanoylglycerol-induced phosphorylation of a 47 kDa protein in human platelets.
Treated thrombin-stimulated platelets with 1 µM staurosporine to measure 47 kDa and 20 kDa protein phosphorylation, ATP and serotonin secretion, aggregation kinetics, and inositol phosphate and phosphatidic acid formation.
Staurosporine (1 µM) caused complete inhibition of dioctanoylglycerol- and thrombin-induced 47 kDa protein phosphorylation and 20 kDa myosin light-chain kinase substrate phosphorylation, whereas other tested inhibitors showed partial or no activity.
Staurosporine inhibited thrombin-stimulated secretion of ATP and 5-hydroxytryptamine and slowed aggregation, but produced no effect on thrombin-induced formation of phosphatidic acid or inositol phosphates.

Cite This Study

Watson et al. (1988) studied this question.

synapsesocial.com/papers/6a77728c4fe2e6ffd8ecadae https://doi.org/10.1042/bj2490345

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Implication

In vitro study demonstrates staurosporine inhibits secretion without altering inositol phosphate levels in human platelets, indicating protein kinase C does not regulate phosphoinositide metabolism.

The action of the protein kinase C inhibitor, staurosporine, on human platelets. Evidence against a regulatory role for protein kinase C in the formation of inositol trisphosphate by thrombin

Discussion

Member takes

Implication

Key Points

Cite This Study

The action of the protein kinase C inhibitor, staurosporine, on human platelets. Evidence against a regulatory role for protein kinase C in the formation of inositol trisphosphate by thrombin

Discussion

Member takes

Implication

Key Points

Cite This Study

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