血栓形成中的PKCs

Pathologie-biologie Pub Date : 2015-12-01 DOI:10.1016/j.patbio.2015.09.001

Y. Zaid , N. Senhaji , A. Naya , C. Fadainia , K. Kojok

{"title":"血栓形成中的PKCs","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":"{\"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}","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

摘要

蛋白激酶C (PKC)家族参与了调节血小板活化的几个生理过程。血小板上表达的PKC的每一种异构体，根据激动剂的性质和浓度，可能具有阳性和/或阴性作用。缺乏PKCα的小鼠体内血栓形成明显减少，而PKCθ−/−对PAR4的聚集表现出抑制作用。另一方面，PKCδ通过与Fyn结合抑制血小板聚集。此外，PKCβ通过与其受体RACK1相互作用，通过α ib β3参与了信号传导的初级阶段，PKCβ似乎参与了GPVI下游的血小板功能。本文综述了最近关于PKC在血小板活化和血栓形成中的作用的观察结果。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

PKCs in thrombus formation

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.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊