Hedin K E, Lim N F, Clapham D E
Department of Pharmacology, Mayo Foundation, Rochester, Minnesota 55905, USA.
Neuron. 1996 Feb;16(2):423-9. doi: 10.1016/s0896-6273(00)80060-4.
Xenopus oocytes injected with GIRK1 mRNA express inwardly rectifying K+ channels resembling IKACh. Yet IKACh, the atrial G protein-regulated ion channel, is a heteromultimer of GIRK1 and CIR. Reasoning that an oocyte protein might be substituting for CIR, we cloned XIR, a CIR homolog endogenously expressed by Xenopus oocytes. Coinjecting XIR and GIRK1 mRNAs produced large, inwardly rectifying K+ currents responsive to m2-muscarinic receptor stimulation. The m2-stimulated currents of oocytes expressing GIRK1 alone decreased 80% after injecting antisense oligonucleotides specific to the 5' untranslated region of XIR, but GIRK1/CIR currents were unaffected. Thus, GIRK1 without XIR or CIR only ineffectively produces currents in oocytes. This result suggests that GIRK1 does not form native homomultimeric channels.
注射了GIRK1信使核糖核酸（mRNA）的非洲爪蟾卵母细胞表达出类似乙酰胆碱激活钾电流（IKACh）的内向整流钾通道。然而，IKACh这种心房G蛋白调节离子通道是GIRK1和CIR的异源多聚体。由于推测卵母细胞中的一种蛋白可能替代了CIR，我们克隆了XIR，它是非洲爪蟾卵母细胞内源性表达的CIR同源物。共注射XIR和GIRK1信使核糖核酸产生了对M2毒蕈碱受体刺激有反应的大的内向整流钾电流。单独表达GIRK1的卵母细胞的M2刺激电流在注射针对XIR 5'非翻译区的反义寡核苷酸后降低了80%，但GIRK1/CIR电流不受影响。因此，没有XIR或CIR的GIRK1在卵母细胞中只能低效地产生电流。这一结果表明GIRK1不会形成天然的同源多聚体通道。
