Suppr超能文献

多磷酸肌醇是否参与血小板活化?

Are polyphosphoinositides involved in platelet activation?

作者信息

Perret B P, Plantavid M, Chap H, Douste-Blazy L

出版信息

Biochem Biophys Res Commun. 1983 Jan 27;110(2):660-7. doi: 10.1016/0006-291x(83)91200-7.

Abstract

In human platelets, the amounts of triphosphoinositides (TPI) and diphosphoinositides (DPI) increase after 30 sec and level off after 120 sec of thrombin stimulation. After 180 sec of thrombin challenge, TPI and DPI increase accounts for 66 and 80%, respectively. Polyphosphoinositide changes roughly parallel the release of N-acetyl-beta-D-glucosaminidase and appear as a later event compared to aggregation and serotonin secretion. It is concluded that an increased phosphorylation of polyphosphoinositides might participate in platelets to the process of stimulus-activation coupling and might be linked to thrombin receptor occupancy. A role of DPI in platelet activation is suggested by the observation that DPI promote platelet aggregation, the mechanism of which is discussed.

摘要

在人血小板中,凝血酶刺激30秒后三磷酸肌醇(TPI)和二磷酸肌醇(DPI)的量增加,120秒后趋于平稳。凝血酶刺激180秒后,TPI和DPI的增加量分别占66%和80%。多磷酸肌醇的变化大致与N-乙酰-β-D-氨基葡萄糖苷酶的释放平行,并且与聚集和5-羟色胺分泌相比是较晚发生的事件。得出的结论是,多磷酸肌醇磷酸化增加可能参与血小板的刺激-激活偶联过程,并且可能与凝血酶受体占据有关。DPI促进血小板聚集这一观察结果提示了DPI在血小板激活中的作用,并对其机制进行了讨论。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验