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Insulin-induced expression of prostacyclin receptors on platelets is mediated through ADP-ribosylation of Gi alpha protein.

机译:胰岛素诱导的血小板上前列环素受体的表达是通过Giα蛋白的ADP-核糖基化介导的。

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摘要

The binding of insulin in physiological amounts to human blood platelets, which increases adenylate cyclase-linked prostacyclin receptor numbers on the cell surface, was found to be directly related to the ADP-ribosylation of the Gi alpha. Conversely, resuspension of the insulin-treated platelets in the hormone-free medium decreased both the prostaglandin receptor numbers and ADP-ribosylation of Gi alpha. Furthermore, incubation of platelets with pertussis toxin or its A-protomer, which ADP-ribosylates Gi alpha, also stimulated the binding of the prostanoid. These results suggest that the increase of prostacyclin receptor numbers in platelets is mediated through the ADP-ribosylation of Gi alpha.
机译:发现生理量的胰岛素与人血小板的结合增加了细胞表面上腺苷酸环化酶连接的前列环素受体的数量,这与Giα的ADP-核糖基化直接相关。相反,将胰岛素处理的血小板重悬于无激素的培养基中会同时降低前列腺素受体数目和Giα的ADP-核糖基化。此外,将血小板与百日咳毒素或其A-protomer(ADP-核糖基化Giα)一起孵育,也会刺激前列腺素的结合。这些结果表明,血小板中前列环素受体数目的增加是通过Giα的ADP-核糖基化介导的。

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