| First Author | Isomoto S | Year | 1996 |
| Journal | Biochem Biophys Res Commun | Volume | 218 |
| Issue | 1 | Pages | 286-91 |
| PubMed ID | 8573147 | Mgi Jnum | J:43383 |
| Mgi Id | MGI:1097581 | Doi | 10.1006/bbrc.1996.0050 |
| Citation | Isomoto S, et al. (1996) A novel ubiquitously distributed isoform of GIRK2 (GIRK2B) enhances GIRK1 expression of the G-protein-gated K+ current in Xenopus oocytes. Biochem Biophys Res Commun 218(1):286-91 |
| abstractText | 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. |
