| pubmed-article:1313452 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1313452 | lifeskim:mentions | umls-concept:C0005821 | lld:lifeskim |
| pubmed-article:1313452 | lifeskim:mentions | umls-concept:C0032173 | lld:lifeskim |
| pubmed-article:1313452 | lifeskim:mentions | umls-concept:C1522642 | lld:lifeskim |
| pubmed-article:1313452 | lifeskim:mentions | umls-concept:C0076552 | lld:lifeskim |
| pubmed-article:1313452 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:1313452 | pubmed:dateCreated | 1992-5-4 | lld:pubmed |
| pubmed-article:1313452 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:1313452 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1313452 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:1313452 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1313452 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:1313452 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:1313452 | pubmed:author | pubmed-author:IshiiKK | lld:pubmed |
| pubmed-article:1313452 | pubmed:author | pubmed-author:OkuYY | lld:pubmed |
| pubmed-article:1313452 | pubmed:author | pubmed-author:HungD TDT | lld:pubmed |
| pubmed-article:1313452 | pubmed:author | pubmed-author:CoughlinS RSR | lld:pubmed |
| pubmed-article:1313452 | pubmed:author | pubmed-author:WheatonV IVI | lld:pubmed |
| pubmed-article:1313452 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1313452 | pubmed:volume | 89 | lld:pubmed |
| pubmed-article:1313452 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1313452 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1313452 | pubmed:pagination | 1350-3 | lld:pubmed |
| pubmed-article:1313452 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1313452 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1313452 | pubmed:articleTitle | Cloned platelet thrombin receptor is necessary for thrombin-induced platelet activation. | lld:pubmed |
| pubmed-article:1313452 | pubmed:affiliation | Department of Laboratory Medicine, University of California, San Francisco 94143. | lld:pubmed |
| pubmed-article:1313452 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1313452 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1313452 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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