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在血小板被胶原蛋白激活的过程中,胞质游离钙离子浓度的升高是由血栓素A2直接引发的。

Elevation of cytosolic free Ca2+ is directly evoked by thromboxane A2 in human platelets during activation with collagen.

作者信息

Moriyama T, Takamura H, Narita H, Tanaka K, Matsuura T, Kito M

机构信息

Research Institute for Food Science, Kyoto University.

出版信息

J Biochem. 1988 Jun;103(6):901-2. doi: 10.1093/oxfordjournals.jbchem.a122383.

Abstract

The thromboxane A2 antagonist, ONO-3708, completely inhibited the increase in cytosolic free Ca2+ in human platelets during activation with collagen. Half-maximal Ca2+ release and influx required about 3 and 4 nM STA2, a stable thromboxane A2 mimetic, respectively. However, half maximal activation of phospholipase C required about 18 nM STA2. This suggests that thromboxane A2 directly causes Ca2+ mobilization without further activation of phospholipase C during activation of human platelets with collagen.

摘要

血栓素A2拮抗剂ONO - 3708能完全抑制胶原激活人血小板过程中胞质游离Ca2+的增加。半最大Ca2+释放和内流分别需要约3 nM和4 nM的STA2(一种稳定的血栓素A2模拟物)。然而,磷脂酶C的半最大激活需要约18 nM的STA2。这表明在用胶原激活人血小板的过程中,血栓素A2直接引起Ca2+动员,而无需进一步激活磷脂酶C。

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