Velimirovic B M, Gordon E A, Lim N F, Navarro B, Clapham D E
Department of Pharmacology, Mayo Foundation, Rochester, MN 55905, USA.
FEBS Lett. 1996 Jan 22;379(1):31-7. doi: 10.1016/0014-5793(95)01465-9.
G protein-activated inwardly rectifying K+ channel subunits GIRK1 (Kir 3.1), GIRK2 (Kir 3.2), and CIR (Kir 3.4) were expressed individually or in combination in Xenopus oocytes and CHO cells. GIRK1 coexpressed with CIR or GIRK2, produced currents up to 10-fold larger than any of the subunits expressed alone. No such clear synergistic effects were observed upon coexpression of CIR/GIRK2 under the same conditions. Coexpression of G protein beta gamma (G beta 1 gamma 2) increased the current through GIRK1/GIRK2 and GIRK2 channels. G beta gamma subunits purified from bovine brain, increased channel activity 50-1000-fold in patches from cells expressing GIRK1/GIRK2 or GIRK2 alone. The single GIRK1/GIRK2 channels resembled previously described neuronal G protein-gated K+ channels. In contrast, single GIRK2 channels were short-lived and unlike any previously described neuronal K+ channel. We propose that some neuronal G protein-activated inward rectifier K+ channels may be formed by a GIRK1/GIRK2 heteromultimer and that G beta gamma activation may involve both subunits.
G蛋白激活的内向整流钾离子通道亚基GIRK1（Kir 3.1）、GIRK2（Kir 3.2）和CIR（Kir 3.4）分别或组合在非洲爪蟾卵母细胞和CHO细胞中表达。GIRK1与CIR或GIRK2共表达时，产生的电流比单独表达的任何一个亚基大10倍。在相同条件下，CIR/GIRK2共表达时未观察到如此明显的协同效应。G蛋白βγ亚基（Gβ1γ2）的共表达增加了通过GIRK1/GIRK2和GIRK2通道的电流。从牛脑中纯化的Gβγ亚基，使表达GIRK1/GIRK2或单独表达GIRK2的细胞片膜中的通道活性增加了50 - 1000倍。单个GIRK1/GIRK2通道类似于先前描述的神经元G蛋白门控钾离子通道。相比之下，单个GIRK2通道寿命短暂，与先前描述的任何神经元钾离子通道都不同。我们提出，一些神经元G蛋白激活的内向整流钾离子通道可能由GIRK1/GIRK2异源多聚体形成，并且Gβγ激活可能涉及两个亚基。
