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    Home > Active Ingredient News > Antitumor Therapy > Blood: Talin1 is the main Rap1 effector for platelet integration activation

    Blood: Talin1 is the main Rap1 effector for platelet integration activation

    • Last Update: 2020-06-16
    • Source: Internet
    • Author: User
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    Rap1 is the main convergence point of platelet signaling pathway, regulating the combination of talin1 and integrated b cytoplasmic domain, thus activating the integrated hormone, promoting platelet aggregation, and achieving effective hemostaticAt present, the natural link between Rap1 and talin1 during the integration hormone activation process is not fully definedPrevious studies have found a low affinity rap1 binding site in the talin1 F0 domain, which has little effect on platelet integration activationRecently, Lagarrigue and others have found another Rap1 binding site in the talin1 F1 domain, and the contribution in the model system is significantly higher than in the F0 domainThe researchers further developed a mouse model that carries the mutation, which blocks the binding of Rap1 without affecting the expression of talin1; only the binding site mutation (R118E) on the talin1 F1 domain can survive, and if the Rap1 binding site in the F0 and F1 domains is mutated at the same time (R35E, R118E), the mice cannot surviveIn platelets, the loss of the interaction of Rap1-talin1 F1 significantly reduces the activation of the talin1-mediated platelets b1 and b3 integratorsThe concentration of integrators and platelet aggregation in mice that only expressed double mutations of the platelets of talin1 (R35E, R118E) were more pronounced, similar to defects observed in platelets that lacked Rap1b and Rap1b at the same timeAlthough Rap1 is important in thrombosis, platelet secretion, and surface exposure to phosphatidylline, the loss of Rap1-talin1 interactions in the platelets of talin1 (R35E, R118E) has little effect on these processesThis study shows that talin1 is the main direct effect of Rap1 GTPases, which regulates platelet integration activation during the hemostatic process
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