G protein-coupled inwardly-rectifying potassium channel: Difference between revisions
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==Examples== | ==Examples== | ||
A wide variety of G protein-coupled receptors activate GIRKs, including the [[muscarinic acetylcholine receptor M2|M<sub>2</sub>-muscarinic]], [[adenosine A1 receptor|A<sub>1</sub>-adenosine]], [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic]], [[dopamine receptor D2|D<sub>2</sub>-dopamine]], [[mu Opioid receptor|μ-]] [[delta Opioid receptor|δ-]], and [[kappa Opioid receptor|κ-]][[opioid receptor|opioid]], [[5-HT1A receptor|5-HT<sub>1A</sub> serotonin]], [[somatostatin receptor|somatostatin]], [[galanin receptor|galanin]], [[metabotropic glutamate receptor|m-Glu]], [[GABAB receptor|GABA<sub>B</sub>]], [[TAAR1]], and [[lysophospholipid receptor|sphingosine-1-phosphate]] receptors.<ref name="pmid9860808"/><ref name="GIRK">{{cite journal |vauthors=Ledonne A, Berretta N, Davoli A, Rizzo GR, Bernardi G, Mercuri NB | title = Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons | journal = Front Syst Neurosci | volume = 5 | issue = | pages = 56 | year = 2011 | pmid = 21772817 | pmc = 3131148 | doi = 10.3389/fnsys.2011.00056 | quote = inhibition of firing due to increased release of dopamine; (b) reduction of D2 and GABAB receptor-mediated inhibitory responses (excitatory effects due to disinhibition); and (c) a direct TA1 receptor-mediated activation of GIRK channels which produce cell membrane hyperpolarization. }}</ref> | A wide variety of G protein-coupled receptors activate GIRKs, including the [[muscarinic acetylcholine receptor M2|M<sub>2</sub>-muscarinic]], [[adenosine A1 receptor|A<sub>1</sub>-adenosine]], [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic]], [[dopamine receptor D2|D<sub>2</sub>-dopamine]], [[mu Opioid receptor|μ-]] [[delta Opioid receptor|δ-]], and [[kappa Opioid receptor|κ-]][[opioid receptor|opioid]], [[5-HT1A receptor|5-HT<sub>1A</sub> serotonin]], [[somatostatin receptor|somatostatin]], [[galanin receptor|galanin]], [[metabotropic glutamate receptor|m-Glu]], [[GABAB receptor|GABA<sub>B</sub>]], [[TAAR1]], [[Cannabinoid receptor type 1|CB<sub>1</sub>]] and [[Cannabinoid receptor type 2|CB<sub>2</sub>]], and [[lysophospholipid receptor|sphingosine-1-phosphate]] receptors.<ref name="pmid9860808"/><ref name="GIRK">{{cite journal |vauthors=Ledonne A, Berretta N, Davoli A, Rizzo GR, Bernardi G, Mercuri NB | title = Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons | journal = Front Syst Neurosci | volume = 5 | issue = | pages = 56 | year = 2011 | pmid = 21772817 | pmc = 3131148 | doi = 10.3389/fnsys.2011.00056 | quote = inhibition of firing due to increased release of dopamine; (b) reduction of D2 and GABAB receptor-mediated inhibitory responses (excitatory effects due to disinhibition); and (c) a direct TA1 receptor-mediated activation of GIRK channels which produce cell membrane hyperpolarization.}}</ref><ref>{{cite journal | vauthors = Svízenská I, Dubový P, Sulcová A | title =Cannabinoid Receptors 1 and 2 (CB1 and CB2), Their Distribution, Ligands and Functional Involvement in Nervous System Structures — A Short Review | journal = Pharmacology Biochemistry and Behavior | volume = 90 | issue = 4 | pages = 501–11 | date = October 2008 | pmid = 18584858 | doi = 10.1016/j.pbb.2008.05.010 }}</ref> | ||
Examples of GIRKs include a subset of potassium channels in the heart, which, when activated by [[parasympathetic]] signals such as [[acetylcholine]] through [[M2 receptors|M2 muscarinic receptors]], causes an outward current of potassium, which slows down the [[heart rate]].<ref name="pmid8521474">{{cite journal |vauthors=Kunkel MT, Peralta EG | title = Identification of domains conferring G protein regulation on inward rectifier potassium channels | journal = Cell | volume = 83 | issue = 3 | pages = 443–9 | year = 1995 | pmid = 8521474 | doi = 10.1016/0092-8674(95)90122-1 }}</ref><ref name="pmid10414308">{{cite journal |vauthors=Wickman K, Krapivinsky G, Corey S, Kennedy M, Nemec J, Medina I, Clapham DE | title = Structure, G protein activation, and functional relevance of the cardiac G protein-gated K<sup>+</sup> channel, I<sub>KACh</sub> | journal = Ann. N. Y. Acad. Sci. | volume = 868 | issue = 1| pages = 386–98 | year = 1999 | pmid = 10414308 | doi = 10.1111/j.1749-6632.1999.tb11300.x| url = http://www.annalsnyas.org/cgi/content/abstract/868/1/386 }}</ref> These are called ''muscarinic potassium channels'' (I<sub>KACh</sub>) and are heterotetramers composed of two [[KCNJ3|GIRK1]] and two [[KCNJ5|GIRK4]] subunits.<ref name="pmid7877685">{{cite journal |vauthors=Krapivinsky G, Gordon EA, Wickman K, Velimirović B, Krapivinsky L, Clapham DE | title = The G-protein-gated atrial K<sup>+</sup> channel I<sub>KACh</sub> is a heteromultimer of two inwardly rectifying K<sup>+</sup>-channel proteins | journal = Nature | volume = 374 | issue = 6518 | pages = 135–41 | year = 1995 | pmid = 7877685 | doi = 10.1038/374135a0 }}</ref><ref name="pmid9478984">{{cite journal |vauthors=Corey S, Krapivinsky G, Krapivinsky L, Clapham DE | title = Number and stoichiometry of subunits in the native atrial G-protein-gated K<sup>+</sup> channel, I<sub>KACh</sub> | journal = J. Biol. Chem. | volume = 273 | issue = 9 | pages = 5271–8 | year = 1998 | pmid = 9478984 | doi = 10.1074/jbc.273.9.5271 }}</ref> | Examples of GIRKs include a subset of potassium channels in the heart, which, when activated by [[parasympathetic]] signals such as [[acetylcholine]] through [[M2 receptors|M2 muscarinic receptors]], causes an outward current of potassium, which slows down the [[heart rate]].<ref name="pmid8521474">{{cite journal |vauthors=Kunkel MT, Peralta EG | title = Identification of domains conferring G protein regulation on inward rectifier potassium channels | journal = Cell | volume = 83 | issue = 3 | pages = 443–9 | year = 1995 | pmid = 8521474 | doi = 10.1016/0092-8674(95)90122-1 }}</ref><ref name="pmid10414308">{{cite journal |vauthors=Wickman K, Krapivinsky G, Corey S, Kennedy M, Nemec J, Medina I, Clapham DE | title = Structure, G protein activation, and functional relevance of the cardiac G protein-gated K<sup>+</sup> channel, I<sub>KACh</sub> | journal = Ann. N. Y. Acad. Sci. | volume = 868 | issue = 1| pages = 386–98 | year = 1999 | pmid = 10414308 | doi = 10.1111/j.1749-6632.1999.tb11300.x| url = http://www.annalsnyas.org/cgi/content/abstract/868/1/386 }}</ref> These are called ''muscarinic potassium channels'' (I<sub>KACh</sub>) and are heterotetramers composed of two [[KCNJ3|GIRK1]] and two [[KCNJ5|GIRK4]] subunits.<ref name="pmid7877685">{{cite journal |vauthors=Krapivinsky G, Gordon EA, Wickman K, Velimirović B, Krapivinsky L, Clapham DE | title = The G-protein-gated atrial K<sup>+</sup> channel I<sub>KACh</sub> is a heteromultimer of two inwardly rectifying K<sup>+</sup>-channel proteins | journal = Nature | volume = 374 | issue = 6518 | pages = 135–41 | year = 1995 | pmid = 7877685 | doi = 10.1038/374135a0 }}</ref><ref name="pmid9478984">{{cite journal |vauthors=Corey S, Krapivinsky G, Krapivinsky L, Clapham DE | title = Number and stoichiometry of subunits in the native atrial G-protein-gated K<sup>+</sup> channel, I<sub>KACh</sub> | journal = J. Biol. Chem. | volume = 273 | issue = 9 | pages = 5271–8 | year = 1998 | pmid = 9478984 | doi = 10.1074/jbc.273.9.5271 }}</ref> |
Revision as of 17:41, 19 May 2018
potassium inwardly-rectifying channel, subfamily J, member 3 | |
---|---|
Identifiers | |
Symbol | KCNJ3 |
Alt. symbols | Kir3.1, GIRK1, KGA |
IUPHAR | 434 |
Entrez | 3760 |
HUGO | 6264 |
OMIM | 601534 |
RefSeq | NM_002239 |
UniProt | P48549 |
Other data | |
Locus | Chr. 2 q24.1 |
potassium inwardly-rectifying channel, subfamily J, member 6 | |
---|---|
Identifiers | |
Symbol | KCNJ6 |
Alt. symbols | KCNJ7, Kir3.2, GIRK2, KATP2, BIR1, hiGIRK2 |
IUPHAR | 435 |
Entrez | 3763 |
HUGO | 6267 |
OMIM | 600877 |
RefSeq | NM_002240 |
UniProt | P48051 |
Other data | |
Locus | Chr. 21 q22.1 |
potassium inwardly-rectifying channel, subfamily J, member 9 | |
---|---|
Identifiers | |
Symbol | KCNJ9 |
Alt. symbols | Kir3.3, GIRK3 |
IUPHAR | 436 |
Entrez | 3765 |
HUGO | 6270 |
OMIM | 600932 |
RefSeq | NM_004983 |
UniProt | Q92806 |
Other data | |
Locus | Chr. 1 q23.2 |
potassium inwardly-rectifying channel, subfamily J, member 5 | |
---|---|
Identifiers | |
Symbol | KCNJ5 |
Alt. symbols | Kir3.4, CIR, KATP1, GIRK4 |
IUPHAR | 437 |
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 hyperpolarization of the cell membrane.[3] G protein-coupled inwardly-rectifying potassium channels are a type of G protein-gated ion channels because of this direct activation of GIRK channels by G protein subunits.
GIRK1 to GIRK3 are distributed broadly in the central nervous system, where their distributions overlap.[4][5][6] GIRK4, instead, is found primarily in the heart.[7]
Subtypes
protein | gene | aliases |
---|---|---|
GIRK1 | KCNJ3 | Kir3.1 |
GIRK2 | KCNJ6 | Kir3.2 |
GIRK3 | KCNJ9 | Kir3.3 |
GIRK4 | KCNJ5 | Kir3.4 |
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, TAAR1, CB1 and CB2, and sphingosine-1-phosphate receptors.[2][3][8]
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.[9][10] These are called muscarinic potassium channels (IKACh) and are heterotetramers composed of two GIRK1 and two GIRK4 subunits.[7][11]
References
- ↑ Dascal N (1997). "Signalling via the G protein-activated K+ channels". Cell. Signal. 9 (8): 551–73. doi:10.1016/S0898-6568(97)00095-8. PMID 9429760.
- ↑ 2.0 2.1 Yamada M, Inanobe A, Kurachi Y (December 1998). "G protein regulation of potassium ion channels". Pharmacological Reviews. 50 (4): 723–60. PMID 9860808.
- ↑ 3.0 3.1 Ledonne A, Berretta N, Davoli A, Rizzo GR, Bernardi G, Mercuri NB (2011). "Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons". Front Syst Neurosci. 5: 56. doi:10.3389/fnsys.2011.00056. PMC 3131148. PMID 21772817.
inhibition of firing due to increased release of dopamine; (b) reduction of D2 and GABAB receptor-mediated inhibitory responses (excitatory effects due to disinhibition); and (c) a direct TA1 receptor-mediated activation of GIRK channels which produce cell membrane hyperpolarization.
- ↑ Kobayashi T, Ikeda K, Ichikawa T, Abe S, Togashi S, Kumanishi T (March 1995). "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". Biochem. Biophys. Res. Commun. 208 (3): 1166–73. doi:10.1006/bbrc.1995.1456. PMID 7702616.
- ↑ Karschin C, Dissmann E, Stühmer W, Karschin A (June 1996). "IRK(1-3) and GIRK(1-4) inwardly rectifying K+ channel mRNAs are differentially expressed in the adult rat brain". J. Neurosci. 16 (11): 3559–70. PMID 8642402.
- ↑ Chen SC, Ehrhard P, Goldowitz D, Smeyne RJ (December 1997). "Developmental expression of the GIRK family of inward rectifying potassium channels: implications for abnormalities in the weaver mutant mouse". Brain Res. 778 (2): 251–64. doi:10.1016/S0006-8993(97)00896-2. PMID 9459542.
- ↑ 7.0 7.1 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:10.1038/374135a0. PMID 7877685.
- ↑ Svízenská I, Dubový P, Sulcová A (October 2008). "Cannabinoid Receptors 1 and 2 (CB1 and CB2), Their Distribution, Ligands and Functional Involvement in Nervous System Structures — A Short Review". Pharmacology Biochemistry and Behavior. 90 (4): 501–11. doi:10.1016/j.pbb.2008.05.010. PMID 18584858.
- ↑ Kunkel MT, Peralta EG (1995). "Identification of domains conferring G protein regulation on inward rectifier potassium channels". Cell. 83 (3): 443–9. doi:10.1016/0092-8674(95)90122-1. 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 (1): 386–98. doi:10.1111/j.1749-6632.1999.tb11300.x. PMID 10414308.
- ↑ 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:10.1074/jbc.273.9.5271. PMID 9478984.
External links
- G+Protein-Coupled+Inwardly-Rectifying+Potassium+Channels at the US National Library of Medicine Medical Subject Headings (MeSH)