Molecular properties of neuronal G-protein-activated inwardly rectifying K+ channels.
- Authors
- Lesage, F; Guillemare, E; Fink, M; Duprat, F; Heurteaux, C; Fosset, M; Romey, G; Barhanin, J; Lazdunski, M
- Year
- 1995
- Journal
- The Journal of biological chemistry
- PMID
- 7499385
- DOI
- 10.1074/jbc.270.48.28660
Four cDNA-encoding G-activated inwardly rectifying K+ channels have been cloned recently (Kubo, Y., Reuveny, E., Slesinger, P. A., Jan, Y. N., and Jan, L. Y. (1993) Nature 364, 802-806; Lesage, F., Duprat, F., Fink, M., Guillemare, E., Coppola, T., Lazdunski, M., and Hugnot, J. P. (1994) FEBS Lett. 353, 37-42; Krapivinsky, G., Gordon, E. A., Wickman, K., Velimirovic, B., Krapivinsky, L., and Clapham, D. E. (1995) Nature 374, 135-141). We report the cloning of a mouse GIRK2 splice variant, noted mGIRK2A. Both channel proteins are functionally expressed in Xenopus oocytes upon injection of their cRNA, alone or in combination with the GIRK1 cRNA. Three GIRK channels, mGIRK1-3, are shown to be present in the brain. Colocalization in the same neurons of mGIRK1 and mGIRK2 supports the hypothesis that native channels are made by an heteromeric subunit assembly. GIRK3 channels have not been expressed successfully, even in the presence of the other types of subunits. However, GIRK3 chimeras with the amino- and carboxyl-terminal of GIRK2 are functionally expressed in the presence of GIRK1. The expressed mGIRK2 and mGIRK1, -2 currents are blocked by Ba2+ and Cs+ ions. They are not regulated by protein kinase A and protein kinase C. Channel activity runs down in inside-out excised patches, and ATP is required to prevent this rundown. Since the nonhydrolyzable ATP analog AMP-PCP is also active and since addition of kinases A and C as well as alkaline phosphatase does not modify the ATP effect, it is concluded that ATP hydrolysis is not required. An ATP binding process appears to be essential for maintaining a functional state of the neuronal inward rectifier K+ channel. A Na+ binding site on the cytoplasmic face of the membrane acts in synergy with the ATP binding site to stabilize channel activity.
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| Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2. | Signorini S et al. | β | 1997 | β |
| Ontogeny of gene expression of Kir channel subunits in the rat. | Karschin C et al. | β | 1997 | β |
| Partial structure, chromosome localization, and expression of the mouse Girk4 gene. | Wickman K et al. | β | 1997 | β |
| Positive and negative coupling of the metabotropic glutamate receptors to a G protein-activated K+ channel, GIRK, in Xenopus oocytes. | Sharon D et al. | β | 1997 | β |
| Protein structures in receptor classification. | Barnard EA | β | 1997 | β |
| RGS8 accelerates G-protein-mediated modulation of K+ currents. | Saitoh O et al. | β | 1997 | β |
| Signalling via the G protein-activated K+ channels. | Dascal N | β | 1997 | β |
| Specific regions of heteromeric subunits involved in enhancement of G protein-gated K+ channel activity. | Chan KW et al. | β | 1997 | β |
| Subunit interactions in the assembly of neuronal Kir3.0 inwardly rectifying K+ channels. | Wischmeyer E et al. | β | 1997 | β |
| TASK, a human background K+ channel to sense external pH variations near physiological pH. | Duprat F et al. | β | 1997 | β |
| The structure, function and distribution of the mouse TWIK-1 K+ channel. | Lesage F et al. | β | 1997 | β |
| A recombinant inwardly rectifying potassium channel coupled to GTP-binding proteins. | Chan KW et al. | β | 1996 | β |
| A regenerative link in the ionic fluxes through the weaver potassium channel underlies the pathophysiology of the mutation. | Silverman SK et al. | β | 1996 | β |
| Control of channel activity through a unique amino acid residue of a G protein-gated inwardly rectifying K+ channel subunit. | Chan KW et al. | β | 1996 | β |
| Dominant negative chimeras provide evidence for homo and heteromultimeric assembly of inward rectifier K+ channel proteins via their N-terminal end. | Fink M et al. | β | 1996 | β |
| Functional analysis of the weaver mutant GIRK2 K+ channel and rescue of weaver granule cells. | Kofuji P et al. | β | 1996 | β |
| Functional effects of the mouse weaver mutation on G protein-gated inwardly rectifying K+ channels. | Slesinger PA et al. | β | 1996 | β |
| GABAB receptor-activated inwardly rectifying potassium current in dissociated hippocampal CA3 neurons. | Sodickson DL et al. | β | 1996 | β |
| Heteromultimerization of G-protein-gated inwardly rectifying K+ channel proteins GIRK1 and GIRK2 and their altered expression in weaver brain. | Liao YJ et al. | β | 1996 | β |
| Localization and interaction of epitope-tagged GIRK1 and CIR inward rectifier K+ channel subunits. | Kennedy ME et al. | β | 1996 | β |
| Na+ activation of the muscarinic K+ channel by a G-protein-independent mechanism. | Sui JL et al. | β | 1996 | β |
| Participation of nucleoside-diphosphate kinase in muscarinic K+ channel activation does not involve GTP formation. | Xu L et al. | β | 1996 | β |
| The transmitter-gated channels: a range of receptor types and structures. | Barnard EA | β | 1996 | β |
| Time resolved kinetics of direct G beta 1 gamma 2 interactions with the carboxyl terminus of Kir3.4 inward rectifier K+ channel subunits. | Doupnik CA et al. | β | 1996 | β |