G protein-coupled inwardly-rectifying potassium channel
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| Identifiers | |
| Symbol | KCNJ3 |
| Alt. Symbols | Kir3.1, GIRK1, KGA |
| Entrez | 3760 |
| HUGO | 6264 |
| OMIM | 601534 |
| RefSeq | NM_002239 |
| UniProt | P48549 |
| Other data | |
| Locus | Chr. 2 q24.1 |
| Identifiers | |
| Symbol | KCNJ6 |
| Alt. Symbols | KCNJ7, Kir3.2, GIRK2, KATP2, BIR1, hiGIRK2 |
| Entrez | 3763 |
| HUGO | 6267 |
| OMIM | 600877 |
| RefSeq | NM_002240 |
| UniProt | P48051 |
| Other data | |
| Locus | Chr. 21 q22.1 |
| Identifiers | |
| Symbol | KCNJ9 |
| Alt. Symbols | Kir3.3, GIRK3 |
| Entrez | 3765 |
| HUGO | 6270 |
| OMIM | 600932 |
| RefSeq | NM_004983 |
| UniProt | Q92806 |
| Other data | |
| Locus | Chr. 1 q23.2 |
| Identifiers | |
| Symbol | KCNJ5 |
| Alt. Symbols | Kir3.4, CIR, KATP1, GIRK4 |
| Entrez | 3762 |
| HUGO | 6266 |
| OMIM | 600734 |
| RefSeq | NM_000890 |
| UniProt | P48544 |
| Other data | |
| Locus | Chr. 11 q24 |
The G protein-coupled inwardly-rectifying potassium channels (GIRKs) are a family of inward-rectifier potassium ion channels which are activated (opened) via a signal transduction cascade starting with ligand stimulated G protein-coupled receptors (GPCRs).[1][2] GPCRs in turn release activated G-protein βγ subunits (Gβγ) from inactive heterotrimeric G protein complexes (Gαβγ). Finally the Gβγ dimeric protein interacts with GIRK channels to open them so that they become permeable to potassium ions resulting in depolarization of the cell.
Contents |
[edit] Subtypes
| protein | gene | aliases |
|---|---|---|
| GIRK1 | KCNJ3 | Kir3.1 |
| GIRK2 | KCNJ6 | Kir3.2 |
| GIRK3 | KCNJ9 | Kir3.3 |
| GIRK4 | KCNJ5 | Kir3.4 |
[edit] Examples
A wide variety of G-protein coupled receptors activate GIRKs including the M2-muscarinic, A1-adenosine, α2-adrenergic, D2-dopamine, μ- δ-, and κ-opioid, 5-HT1A serotonin, somatostatin, galanin, m-Glu, GABAB, and sphingosine-1-phosphate receptors.[2]
Examples of GIRKs include a subset of potassium channels in the heart which when activated by parasympathetic signals such as acetylcholine through M2 muscarinic receptors, causes an outward current of potassium which slows down the heart rate.[3][4] These are called muscarinic potassium channels (IKACh) and are heterotetramers comprised of two GIRK1 and two GIRK4 subunits.[5][6]
[edit] References
- ^ Dascal N (1997). "Signalling via the G protein-activated K+ channels". Cell. Signal. 9 (8): 551–73. doi:. PMID 9429760.
- ^ a b Yamada M, Inanobe A, Kurachi Y (1998). "G protein regulation of potassium ion channels". Pharmacol. Rev. 50 (4): 723–60. PMID 9860808.
- ^ Kunkel MT, Peralta EG (1995). "Identification of domains conferring G protein regulation on inward rectifier potassium channels". Cell 83 (3): 443–9. doi:. PMID 8521474.
- ^ Wickman K, Krapivinsky G, Corey S, Kennedy M, Nemec J, Medina I, Clapham DE (1999). "Structure, G protein activation, and functional relevance of the cardiac G protein-gated K+ channel, IKACh". Ann. N. Y. Acad. Sci. 868: 386–98. PMID 10414308.
- ^ Krapivinsky G, Gordon EA, Wickman K, Velimirović B, Krapivinsky L, Clapham DE (1995). "The G-protein-gated atrial K+ channel IKACh is a heteromultimer of two inwardly rectifying K+-channel proteins". Nature 374 (6518): 135–41. doi:. PMID 7877685.
- ^ Corey S, Krapivinsky G, Krapivinsky L, Clapham DE (1998). "Number and stoichiometry of subunits in the native atrial G-protein-gated K+ channel, IKACh". J. Biol. Chem. 273 (9): 5271–8. doi:. PMID 9478984.
[edit] External links
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