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[G(i)蛋白对肌醇-1,4,5-三磷酸受体的调控]

[Regulation of inositol-1,4,5-triphosphate receptor by G(i)-protein].

作者信息

Nikashin A B, Neylon K B, Bobik A, Tkachuk V A

机构信息

Cardiological Research-Industrial Complex, Moscow, Russia.

出版信息

Ross Fiziol Zh Im I M Sechenova. 1999 Aug;85(8):1011-21.

PMID:10643593
Abstract

The pertussis toxin (PT) inhibits thrombin-induced mobilising of Ca2+ but does not affect formation of inositol-1, 4, 5-triphosphate (IPh3). The latter being related to Gi and G0, the possibility of a direct effect of these proteins on the IPh3-induced release of Ca2+ from sarcoplasmic reticulum, was studied. The data obtained suggest existence of an association of the Gi3 protein with the IPh3-P on the sarcoplasmic reticulum membrane, as well as a direct modulation by the Gi protein of the Ca2+ release from intracellular stores.

摘要

百日咳毒素(PT)可抑制凝血酶诱导的钙离子动员,但不影响肌醇-1,4,5-三磷酸(IP3)的形成。由于后者与Gi和G0相关,因此研究了这些蛋白质对IP3诱导的肌浆网钙离子释放的直接作用的可能性。所获得的数据表明,Gi3蛋白与肌浆网膜上的IP3-P存在关联,并且Gi蛋白可直接调节细胞内钙库的钙离子释放。

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