Y. Zaid , N. Senhaji , A. Naya , C. Fadainia , K. Kojok
{"title":"PKCs in thrombus formation","authors":"Y. Zaid , N. Senhaji , A. Naya , C. Fadainia , K. Kojok","doi":"10.1016/j.patbio.2015.09.001","DOIUrl":null,"url":null,"abstract":"<div><p>The protein kinase C (PKC) family has been implicated in several physiological processes regulating platelet activation. Each isoform of PKC expressed on platelets, may have a positive and/or negative role depending on the nature and concentration of the agonist. Mice lacking PKCα show much reduced thrombus formation <em>in vivo</em>, while PKCθ<sup>−/−</sup> showed inhibition of aggregation in response to PAR4. On the other hand, PKCδ by associating with Fyn, inhibits platelet aggregation. In addition, PKCβ by interacting with its receptor RACK1 has been implicated in the primary phases of signaling <em>via</em> the αIIbβ3 and finally PKCɛ appears to be involved in platelet function downstream GPVI. The present review discusses the latest observations relevant to the role of individual PKC isoforms in platelet activation and thrombus formation.</p></div>","PeriodicalId":19743,"journal":{"name":"Pathologie-biologie","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.patbio.2015.09.001","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pathologie-biologie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0369811415000954","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
Abstract
The protein kinase C (PKC) family has been implicated in several physiological processes regulating platelet activation. Each isoform of PKC expressed on platelets, may have a positive and/or negative role depending on the nature and concentration of the agonist. Mice lacking PKCα show much reduced thrombus formation in vivo, while PKCθ−/− showed inhibition of aggregation in response to PAR4. On the other hand, PKCδ by associating with Fyn, inhibits platelet aggregation. In addition, PKCβ by interacting with its receptor RACK1 has been implicated in the primary phases of signaling via the αIIbβ3 and finally PKCɛ appears to be involved in platelet function downstream GPVI. The present review discusses the latest observations relevant to the role of individual PKC isoforms in platelet activation and thrombus formation.
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