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二磷酸腺苷(ADP)刺激人体血小板中肌醇三磷酸(IP3)的形成。

ADP stimulates IP3 formation in human platelets.

作者信息

Daniel J L, Dangelmaier C A, Selak M, Smith J B

出版信息

FEBS Lett. 1986 Oct 6;206(2):299-303. doi: 10.1016/0014-5793(86)81000-6.

Abstract

Aspirinated human platelets labeled with 32PO4 showed a 1.7-fold increase in [32P]IP3 when stimulated with ADP. ADP-stimulated mobilization of internal Ca2+ and phosphorylation of myosin were enhanced in the presence of extracellular Ca2+ but the increase in IP3 was not significantly affected by external Ca2+. The Ca2+ ionophore, ionomycin, elevated internal Ca2+ and induced myosin phosphorylation without a detectable change in IP3. These results indicate that the mechanism of ADP stimulation of human platelets is similar to that of other platelet agonists and supports the theory that IP3 functions to liberate internal Ca2+.

摘要

用32PO4标记的经阿司匹林处理的人血小板在受到ADP刺激时,[32P]IP3增加了1.7倍。在细胞外Ca2+存在的情况下,ADP刺激的细胞内Ca2+动员和肌球蛋白磷酸化增强,但IP3的增加不受细胞外Ca2+的显著影响。Ca2+离子载体离子霉素升高了细胞内Ca2+并诱导了肌球蛋白磷酸化,而IP3没有可检测到的变化。这些结果表明,ADP刺激人血小板的机制与其他血小板激动剂相似,并支持IP3起释放细胞内Ca2+作用的理论。

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