无细胞血小板膜系统中的刺激-反应偶联。凝血酶诱导的GTP依赖性Ca2+释放，以及百日咳毒素和一种阻断IP3介导的钙释放的单克隆抗体的抑制作用。
Stimulus-response coupling in a cell-free platelet membrane system. GTP-dependent release of Ca2+ by thrombin, and inhibition by pertussis toxin and a monoclonal antibody that blocks calcium release by IP3.
作者信息
O'Rourke F, Zavoico G B, Smith L H, Feinstein M B
出版信息
FEBS Lett. 1987 Apr 6;214(1):176-80. doi: 10.1016/0014-5793(87)80037-6.
The Ca2+-mobilizing action of thrombin was demonstrated in a cell-free platelet membrane system consisting of open sheets of plasma membrane plus sealed membrane vesicles that accumulate Ca2+ and release Ca2+ in response to IP3. Thrombin plus GTP, acting on plasma membrane (not vesicles), produced a soluble factor (destroyed by alkaline phosphatase) that released Ca2+ from the vesicles. This effect of thrombin/GTP was blocked by a monoclonal antibody that binds to vesicles and prevents Ca2+ release by IP3. Pertussis toxin plus NAD ADP-ribosylated plasma membrane polypeptides of 39 and 41 kDa and blocked Ca2+ release by thrombin/GTP, but not by IP3.
凝血酶的钙离子动员作用在一个无细胞血小板膜系统中得到证实，该系统由质膜开放片层加上密封膜囊泡组成，这些膜囊泡可积累钙离子并响应肌醇三磷酸（IP3）释放钙离子。凝血酶加鸟苷三磷酸（GTP）作用于质膜（而非囊泡），产生一种可溶性因子（被碱性磷酸酶破坏），该因子可从囊泡中释放钙离子。凝血酶/GTP的这种作用被一种单克隆抗体阻断，该抗体与囊泡结合并阻止IP3介导的钙离子释放。百日咳毒素加烟酰胺腺嘌呤二核苷酸（NAD）使39 kDa和41 kDa的质膜多肽发生ADP核糖基化，并阻断凝血酶/GTP介导的钙离子释放，但不阻断IP3介导的钙离子释放。
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