血小板激活因子（1-O-十六烷基/十八烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）诱导的纤维蛋白原与血小板的结合依赖于代谢能量。
PAF-acether (1-O-hexadecyl/octadecyl-2-acetyl-sn-glycero-3-phosphocholine)-induced fibrinogen binding to platelets depends on metabolic energy.
作者信息
Kloprogge E, Hasselaar P, Akkerman J W
出版信息
Biochem J. 1986 Sep 15;238(3):885-91. doi: 10.1042/bj2380885.
Abstract
A combination of CN- and 2-deoxy-D-glucose decreases the binding of fibrinogen to platelets stimulated with PAF-acether (1-O-hexadecyl/octadecyl-2-acetyl-sn-glycero-3-phosphocholine). Decreased binding is found after pretreatment with metabolic inhibitors, thereby lowering the energy content before stimulation as well as at various stages after stimulation of undisturbed cells. Binding and ATP hydrolysis occur in parallel, suggesting tight coupling between both phenomena. Energy appears to be predominantly required for exposure and maintenance of accessible binding sites, whereas the interaction between fibrinogen and the exposed sites does not depend on metabolic energy.
摘要
氰离子（CN-）与2-脱氧-D-葡萄糖的组合可降低纤维蛋白原与由血小板激活因子（1-O-十六烷基/十八烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）刺激的血小板的结合。在用代谢抑制剂预处理后发现结合减少，从而降低了未受干扰细胞在刺激前以及刺激后各个阶段的能量含量。结合与ATP水解同时发生，表明这两种现象之间紧密偶联。能量似乎主要用于暴露和维持可及的结合位点，而纤维蛋白原与暴露位点之间的相互作用并不依赖于代谢能量。
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