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Research Article Free access | 10.1172/JCI115721

Cloned platelet thrombin receptor is necessary for thrombin-induced platelet activation.

D T Hung, T K Vu, V I Wheaton, K Ishii, and S R Coughlin

Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Vu, T. in: JCI | PubMed | Google Scholar

Department of Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Wheaton, V. in: JCI | PubMed | Google Scholar

Department of Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Ishii, K. in: JCI | PubMed | Google Scholar

Department of Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Coughlin, S. in: JCI | PubMed | Google Scholar

Published April 1, 1992 - More info

Published in Volume 89, Issue 4 on April 1, 1992
J Clin Invest. 1992;89(4):1350–1353. https://doi.org/10.1172/JCI115721.
© 1992 The American Society for Clinical Investigation
Published April 1, 1992 - Version history
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Abstract

Platelet activation by thrombin is critical for hemostasis and thrombosis. Structure-function studies with a recently cloned platelet thrombin receptor suggest that a hirudin-like domain in the receptor's extracellular amino terminal extension is a thrombin-binding determinant important for receptor activation. We now report that a peptide antiserum to this domain is a potent and specific antagonist of thrombin-induced platelet activation. This study demonstrates that the cloned platelet thrombin receptor is necessary for platelet activation by thrombin, and provides a strategy for developing blocking monoclonal antibodies of potential therapeutic value.

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