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Identification of regions that regulate the expression and activity of G protein-gated inward rectifier K+ channels in Xenopus oocytes.
Stevens EB
,
Woodward R
,
Ho IH
,
Murrell-Lagnado R
.
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1. The involvement of the cytoplasmic and core regions of K+ channel Kir3.1 and Kir3.2 subunits in determining the cell surface expression and G protein-gated activity of homomeric and heteromeric channel complexes was investigated by heterologous expression of chimeric and wild-type subunits together with the m2 muscarinic receptor in Xenopus oocytes. 2. Co-expression of Kir3.1 and Kir3.2 subunits yielded currents severalfold larger than those elicited by the individual expression of these subunits. Immunofluorescence labelling indicated that Kir3.2 homomeric channels and Kir3.1-Kir3.2 heteromeric channels were expressed at high levels at the cell surface whereas Kir3.1 homomeric complexes were not expressed at the cell surface. Chimeric subunits composed of Kir3.1 and Kir3.2 showed that the presence of either the cytoplasmic tails or the core region of Kir3.1 in all subunits inhibits expression of channels at the plasma membrane. 3. Substituting the cytoplasmic tails of Kir3.1 for the cytoplasmic tails of Kir3.2, generated a chimeric subunit (121) which displayed dramatically increased acetylcholine-induced channel activity compared with the wild-type Kir3.2 homomeric channel. Cell-attached, single-channel recordings revealed that chimera 121 channel openings were longer than Kir3.2 openings. 4. Individually substituting the N- and C-terminal tails of Kir3.1 for those of Kir3.2 showed that the C-terminal tail of Kir3.1 enhanced the activity of heteromeric channels independently of the N-terminal or core regions of this subunit. 5. The chimeric channel, 121, displayed a higher ratio of ACh-induced to basal activity than the Kir3.1-Kir3.2 or Kir3.2 channels. A smaller proportion of chimera 121 channels appear to be activated by the basal turnover of G proteins, implying that they have a lower affinity for G beta gamma. Our results suggest that substituting the Kir3.1 C-terminal tail for the Kir3.2tail promotes the opening conformational change of the G beta gamma-bound channel. 6. The core and C-terminal regions of Kir3.1 independently conferred time dependence on voltage-dependent activation. The time constant (tau) was between 5 and 10 ms and varied little over the voltage range -60 to -120 mV.
Bond,
Cloning and functional expression of the cDNA encoding an inwardly-rectifying potassium channel expressed in pancreatic beta-cells and in the brain.
1995, Pubmed,
Xenbase
Bond,
Cloning and functional expression of the cDNA encoding an inwardly-rectifying potassium channel expressed in pancreatic beta-cells and in the brain.
1995,
Pubmed
,
Xenbase
Chan,
Control of channel activity through a unique amino acid residue of a G protein-gated inwardly rectifying K+ channel subunit.
1996,
Pubmed
,
Xenbase
Chan,
Specific regions of heteromeric subunits involved in enhancement of G protein-gated K+ channel activity.
1997,
Pubmed
,
Xenbase
Chan,
A recombinant inwardly rectifying potassium channel coupled to GTP-binding proteins.
1996,
Pubmed
,
Xenbase
Dascal,
Atrial G protein-activated K+ channel: expression cloning and molecular properties.
1993,
Pubmed
,
Xenbase
Duprat,
Heterologous multimeric assembly is essential for K+ channel activity of neuronal and cardiac G-protein-activated inward rectifiers.
1995,
Pubmed
,
Xenbase
Fink,
A new K+ channel beta subunit to specifically enhance Kv2.2 (CDRK) expression.
1996,
Pubmed
,
Xenbase
Glowatzki,
Subunit-dependent assembly of inward-rectifier K+ channels.
1995,
Pubmed
,
Xenbase
Hedin,
Cloning of a Xenopus laevis inwardly rectifying K+ channel subunit that permits GIRK1 expression of IKACh currents in oocytes.
1996,
Pubmed
,
Xenbase
Huang,
Evidence that direct binding of G beta gamma to the GIRK1 G protein-gated inwardly rectifying K+ channel is important for channel activation.
1995,
Pubmed
,
Xenbase
Huang,
Binding of the G protein betagamma subunit to multiple regions of G protein-gated inward-rectifying K+ channels.
1997,
Pubmed
Inanobe,
G beta gamma directly binds to the carboxyl terminus of the G protein-gated muscarinic K+ channel, GIRK1.
1995,
Pubmed
Keller,
Involvement of the chaperone protein calnexin and the acetylcholine receptor beta-subunit in the assembly and cell surface expression of the receptor.
1996,
Pubmed
Kennedy,
Localization and interaction of epitope-tagged GIRK1 and CIR inward rectifier K+ channel subunits.
1996,
Pubmed
,
Xenbase
Kobayashi,
Molecular cloning of a mouse G-protein-activated K+ channel (mGIRK1) and distinct distributions of three GIRK (GIRK1, 2 and 3) mRNAs in mouse brain.
1995,
Pubmed
Kofuji,
Functional analysis of the weaver mutant GIRK2 K+ channel and rescue of weaver granule cells.
1996,
Pubmed
,
Xenbase
Kofuji,
A unique P-region residue is required for slow voltage-dependent gating of a G protein-activated inward rectifier K+ channel expressed in Xenopus oocytes.
1996,
Pubmed
,
Xenbase
Kofuji,
Evidence that neuronal G-protein-gated inwardly rectifying K+ channels are activated by G beta gamma subunits and function as heteromultimers.
1995,
Pubmed
,
Xenbase
Krapivinsky,
G beta gamma binds directly to the G protein-gated K+ channel, IKACh.
1995,
Pubmed
Krapivinsky,
The G-protein-gated atrial K+ channel IKACh is a heteromultimer of two inwardly rectifying K(+)-channel proteins.
1995,
Pubmed
,
Xenbase
Kubo,
Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel.
1993,
Pubmed
,
Xenbase
Kunkel,
Identification of domains conferring G protein regulation on inward rectifier potassium channels.
1995,
Pubmed
,
Xenbase
Lesage,
Molecular properties of neuronal G-protein-activated inwardly rectifying K+ channels.
1995,
Pubmed
,
Xenbase
Lesage,
Cloning provides evidence for a family of inward rectifier and G-protein coupled K+ channels in the brain.
1994,
Pubmed
,
Xenbase
Logothetis,
The beta gamma subunits of GTP-binding proteins activate the muscarinic K+ channel in heart.
,
Pubmed
Lopatin,
The mechanism of inward rectification of potassium channels: "long-pore plugging" by cytoplasmic polyamines.
1995,
Pubmed
,
Xenbase
Navarro,
Nonselective and G betagamma-insensitive weaver K+ channels.
1996,
Pubmed
Patil,
A potassium channel mutation in weaver mice implicates membrane excitability in granule cell differentiation.
1995,
Pubmed
Pessia,
Contributions of the C-terminal domain to gating properties of inward rectifier potassium channels.
1995,
Pubmed
Signorini,
Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2.
1997,
Pubmed
Slesinger,
Identification of structural elements involved in G protein gating of the GIRK1 potassium channel.
1995,
Pubmed
,
Xenbase
Slesinger,
Functional effects of the mouse weaver mutation on G protein-gated inwardly rectifying K+ channels.
1996,
Pubmed
,
Xenbase
Tucker,
Muscarine-gated K+ channel: subunit stoichiometry and structural domains essential for G protein stimulation.
1996,
Pubmed
,
Xenbase
Velimirovic,
The K+ channel inward rectifier subunits form a channel similar to neuronal G protein-gated K+ channel.
1996,
Pubmed
,
Xenbase
Wickman,
Recombinant G-protein beta gamma-subunits activate the muscarinic-gated atrial potassium channel.
1994,
Pubmed
Woodward,
Molecular determinants for assembly of G-protein-activated inwardly rectifying K+ channels.
1997,
Pubmed
,
Xenbase
Yang,
Determination of the subunit stoichiometry of an inwardly rectifying potassium channel.
1995,
Pubmed
,
Xenbase
Yang,
Control of rectification and permeation by residues in two distinct domains in an inward rectifier K+ channel.
1995,
Pubmed
,
Xenbase