Sultan C, Breton M, Mauco G, Grondin P, Plantavid M, Chap H
INSERM Unité 326, Hôpital Purpan, Toulouse, France.
Biochem J. 1990 Aug 1;269(3):831-4. doi: 10.1042/bj2690831.
Radioactive PtdIns(3)P was detected in human platelets incubated with [32P]Pi, but remained unaffected by thrombin treatment. In contrast, [32P]PtdIns(3,4)P2 was absent from resting platelets, but was produced by thrombin-activated platelets in a dose- and time-dependent manner. [32P]PtdInsP3 was never found under these conditions. These changes are similar to those elicited in other cells by platelet-derived growth factor or the oncogene product pp60c-src.
在用[32P]Pi孵育的人血小板中检测到放射性磷脂酰肌醇-3-磷酸(PtdIns(3)P),但其不受凝血酶处理的影响。相比之下,静息血小板中不存在[32P]磷脂酰肌醇-3,4-二磷酸(PtdIns(3,4)P2),但凝血酶激活的血小板以剂量和时间依赖性方式产生[32P]PtdIns(3,4)P2。在这些条件下从未发现[32P]磷脂酰肌醇-3,4,5-三磷酸(PtdInsP3)。这些变化类似于血小板衍生生长因子或癌基因产物pp60c-src在其他细胞中引起的变化。