Kralisz U, Cierniewski C S
Department of Biophysics, Medical University of Lódź, Poland.
Biochem Mol Biol Int. 1998 Jul;45(4):735-43.
To detect whether 125I-alpha IIb beta 3 is associated with tyrosine kinases in platelets, antibodies specific to pp60c-src, pp54/58lyn, and pp62Fyn were used to precipitate their homologous antigens. In contrast to Lyn and Fyn kinases, pp60c-src appears to be complexed with alpha IIb beta 3. Both proteins, pp60c-src and alpha IIb beta 3, coprecipitated when antibodies to pp60c-src were used in the immunoprecipitation experiments. This conclusion was further supported by immunoprecipitation of alpha IIb beta 3 from Triton X-100 extracts of nonlabelled platelets with P2 antibodies. There was no pp60c-src detectable in immunoprecipitates obtained with antibodies specific to alpha 2 beta 1 or GPIb. Since PGE1 was used to prevent platelet activation in buffers throughout all procedures and there was no phosphorylation of pp72syk we assume that the platelets were in the resting state. Therefore, we conclude that alpha IIb beta 3 and pp60c-src can form a complex in resting platelets suggesting that pp60c-src is directly involved in initiating the outside-in signaling cascades in blood platelets.
为检测¹²⁵I-αⅡbβ₃是否与血小板中的酪氨酸激酶相关,使用了针对pp60c-src、pp54/58lyn和pp62Fyn的特异性抗体来沉淀其同源抗原。与Lyn和Fyn激酶不同,pp60c-src似乎与αⅡbβ₃形成复合物。当在免疫沉淀实验中使用针对pp60c-src的抗体时,pp60c-src和αⅡbβ₃这两种蛋白都发生了共沉淀。用P2抗体从未标记血小板的Triton X-100提取物中免疫沉淀αⅡbβ₃进一步支持了这一结论。在用针对α2β1或GPIb的特异性抗体获得的免疫沉淀物中未检测到pp60c-src。由于在所有步骤中均使用前列腺素E1来防止缓冲液中的血小板活化,且pp72syk没有磷酸化,我们假定血小板处于静息状态。因此,我们得出结论,αⅡbβ₃和pp60c-src可以在静息血小板中形成复合物,这表明pp60c-src直接参与启动血小板中的外向内信号级联反应。