Heteromultimerization of G-protein-gated inwardly rectifying K+ channel proteins GIRK1 and GIRK2 and their altered expression in weaver brain.
paper
Cited
Public
Unavailable
- Authors
- Liao, Y J; Jan, Y N; Jan, L Y
- Year
- 1996
- Journal
- The Journal of neuroscience : the official journal of the Society for Neuroscience
- PMID
- 8929423
- DOI
- 10.1523/JNEUROSCI.16-22-07137.1996
- PMCID
- PMC6578936
The weaver (wv) gene (GIRK2) is a member of the G-protein-gated inwardly rectifying potassium (GIRK) channel family, known effectors in the signal transduction pathway of neurotransmitters such as acetylcholine, dopamine, opioid peptides, and substance P in modulation of neurotransmitter release and neuronal excitability. GIRK2 immunoreactivity is found in but not limited to brain regions known to be affected in wv mice, such as the cerebellar granule cells and dopaminergic neurons in the substantia nigra pars compacta. It is also observed in the ventral tegmental area, hippocampus, cerebral cortex, and thalamus. GIRK2 and GIRK1, a related family member, have overlapping yet distinct distributions in rat and mouse brains. In regions where both channel proteins are expressed, such as the cerebral cortex, hippocampus, and cerebellum, they can be co-immunoprecipitated, indicating that they interact to form heteromeric channels in vivo. In the brain of the wv mouse, GIRK2 expression is decreased dramatically. In regions where GIRK1 and GIRK2 distributions overlap, both GIRK1 and GIRK2 expressions are severely disrupted, probably because of their co-assembly. The expression patterns of these GIRK channel subunits provide a basis for consideration of the machinery for neuronal signaling as well as the differential effects of the wv mutation in various neurons.
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| Orchestration of neuronal migration by activity of ion channels, neurotransmitter receptors, and intracellular Ca2+ fluctuations. | Komuro H et al. | β | 1998 | β |
| Pore mutation in a G-protein-gated inwardly rectifying K+ channel subunit causes loss of K+-dependent inhibition in weaver hippocampus. | Jarolimek W et al. | β | 1998 | β |
| The development of voltage-gated ion channels and its relation to activity-dependent development events. | Moody WJ | β | 1998 | β |
| Activation of heteromeric G protein-gated inward rectifier K+ channels overexpressed by adenovirus gene transfer inhibits the excitability of hippocampal neurons. | Ehrengruber MU et al. | β | 1997 | β |
| Binding of the G protein betagamma subunit to multiple regions of G protein-gated inward-rectifying K+ channels. | Huang CL et al. | β | 1997 | β |
| Defective gamma-aminobutyric acid type B receptor-activated inwardly rectifying K+ currents in cerebellar granule cells isolated from weaver and Girk2 null mutant mice. | Slesinger PA et al. | β | 1997 | β |
| Developmental expression of the GIRK family of inward rectifying potassium channels: implications for abnormalities in the weaver mutant mouse. | Chen SC et al. | β | 1997 | β |
| Diverse cell death pathways result from a single missense mutation in weaver mouse. | Migheli A et al. | β | 1997 | β |
| Failed cell migration and death of purkinje cells and deep nuclear neurons in the weaver cerebellum. | Maricich SM et al. | β | 1997 | β |
| G protein-coupled inwardly rectifying K+ channels (GIRKs) mediate postsynaptic but not presynaptic transmitter actions in hippocampal neurons. | LΓΌscher C et al. | β | 1997 | β |
| 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 |
| Potassium channelopathies. | Sanguinetti MC et al. | β | 1997 | β |
| Receptor-regulated ion channels. | Jan LY et al. | β | 1997 | β |
| Signalling via the G protein-activated K+ channels. | Dascal N | β | 1997 | β |
| Subunit stoichiometry of the pancreatic beta-cell ATP-sensitive K+ channel. | Inagaki N et al. | β | 1997 | β |
| Voltage-gated and inwardly rectifying potassium channels. | Jan LY et al. | β | 1997 | β |