Isomoto S, Kondo C, Takahashi N, Matsumoto S, Yamada M, Takumi T, Horio Y, Kurachi Y
Department of Pharmacology II, Faculty of Medicine, Osaka University, Japan.
Biochem Biophys Res Commun. 1996 Jan 5;218(1):286-91. doi: 10.1006/bbrc.1996.0050.
We have isolated a novel variant form of GIRK2, designated GIRK2B, from mouse brain cDNA library. GIRK2B was much shorter than the first type of GIRK2 (GIRK2A), but its amino acid sequence was identical to the corresponding part of GIRK2A except the C-terminal eight amino acid residues. When GIRK2B cRNA was co-injected with GIRK1 and m2-receptor cRNAs to Xenopus oocytes, acetylcholine-induction of the inwardly rectifying K+ current was enhanced dramatically. This suggests that GIRK2B can form a heteromultimeric G-protein-gated K+ channel with GIRK1. The reverse transcription polymerase chain reaction analysis showed that GIRK2B mRNA distributed much more broadly than GIRK1 mRNA. Therefore, GIRK2B might also play other unrecognized roles in various tissues than to form a K+ channel with GIRK1.
我们从小鼠脑cDNA文库中分离出一种新型的GIRK2变异体,命名为GIRK2B。GIRK2B比第一种类型的GIRK2(GIRK2A)短得多,但其氨基酸序列与GIRK2A的相应部分相同,除了C末端的八个氨基酸残基。当将GIRK2B cRNA与GIRK1和m2受体cRNA共同注射到非洲爪蟾卵母细胞中时,乙酰胆碱诱导的内向整流钾电流显著增强。这表明GIRK2B可以与GIRK1形成异源多聚体G蛋白门控钾通道。逆转录聚合酶链反应分析表明,GIRK2B mRNA的分布比GIRK1 mRNA广泛得多。因此,GIRK2B可能在各种组织中发挥其他未被认识的作用,而不仅仅是与GIRK1形成钾通道。