Direct activation of mammalian atrial muscarinic potassium channels by GTP regulatory protein Gk.

Direct activation of mammalian atrial muscarinic potassium channels by GTP regulatory protein Gk.
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GTP 调节蛋白 Gk 直接激活哺乳动物心房毒蕈碱钾通道。

DOI:
10.1126/science.2432660
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发表时间:
1987
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Birnbaumer,L
Birnbaumer,L
中科院分区:
--
文献类型:
--
作者:
Yatani,A;Codina,J;Brown,AM;Birnbaumer,L

文献摘要

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哺乳动物的心率由迷走神经调节,迷走神经通过毒蕈碱乙酰胆碱受体起作用,引起心房起搏细胞的超极化。超极化是由钾通道的开放产生的,并且涉及中间的鸟苷三磷酸结合调节(G)蛋白。心房细胞分离的、由内而外的膜斑中的钾通道现在被证明可被纯化的百日咳毒素敏感性G蛋白激活,G蛋白的亚基组成为αβγ,α亚基为40,000道尔顿。因此,哺乳动物心房毒蕈碱钾通道直接被G蛋白激活,而不是间接通过级联的中间事件。调节这些通道的G蛋白被鉴定为有效的Gk;它在0.2至1 pM时具有活性。因此,酶以外的蛋白质可以在受体偶联G蛋白的控制下。
The mammalian heart rate is regulated by the vagus nerve, which acts via muscarinic acetylcholine receptors to cause hyperpolarization of atrial pacemaker cells. The hyperpolarization is produced by the opening of potassium channels and involves an intermediary guanosine triphosphate-binding regulatory (G) protein. Potassium channels in isolated, inside-out patches of membranes from atrial cells now are shown to be activated by a purified pertussis toxin-sensitive G protein of subunit composition αβγ, with an α subunit of 40,000 daltons. Thus, mammalian atrial muscarinic potassium channels are activated directly by a G protein, not indirectly through a cascade of intermediary events. The G protein regulating these channels is identified as a potent Gk; it is active at 0.2 to 1 pM. Thus, proteins other than enzymes can be under control of receptor coupling G proteins.