Yatani A, Codina J, Brown A M, Birnbaumer L
Science. 1987 Jan 9;235(4785):207-11. doi: 10.1126/science.2432660.
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 alpha beta gamma, with an alpha 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.
哺乳动物的心率受迷走神经调节，迷走神经通过毒蕈碱型乙酰胆碱受体起作用，导致心房起搏细胞超极化。超极化是由钾通道开放产生的，涉及一种中间的鸟苷三磷酸结合调节（G）蛋白。现已表明，从心房细胞分离得到的内翻式膜片上的钾通道可被一种纯化的百日咳毒素敏感的G蛋白激活，该G蛋白的亚基组成为αβγ，其中α亚基的分子量为40,000道尔顿。因此，哺乳动物心房毒蕈碱性钾通道是由G蛋白直接激活的，而非通过一系列中间事件间接激活。调节这些通道的G蛋白被鉴定为一种有效的Gk；它在0.2至1 pM时具有活性。因此，除酶以外的蛋白质也可受与受体偶联的G蛋白的调控。
