KCNJ8: Difference between revisions

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{{Underlinked|date=December 2012}}
{{Infobox_gene}}
{{Infobox_gene}}
'''Potassium inwardly-rectifying channel, subfamily J, member 8''', also known as '''KCNJ8''', is a human [[gene]] encoding the '''K<sub>ir</sub>6.1''' protein.<ref name="entrez">{{cite web | title = Entrez Gene: KCNJ8 potassium inwardly-rectifying channel, subfamily J, member 8| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3764| accessdate = }}</ref> A mutation in KCNJ8 has been associated with cardiac arrest in the early repolarization syndrome.
'''Potassium inwardly-rectifying channel, subfamily J, member 8''', also known as '''KCNJ8''', is a human [[gene]] encoding the '''K<sub>ir</sub>6.1''' [[protein]].<ref name="entrez">{{cite web | title = Entrez Gene: KCNJ8 potassium inwardly-rectifying channel, subfamily J, member 8| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3764| accessdate = }}</ref> A [[mutation]] in KCNJ8 has been associated with [[cardiac arrest]] in the early repolarization syndrome.


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| summary_text = Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. K<sub>ir</sub>6.1 is an integral membrane protein and inward-rectifier type potassium channel. K<sub>ir</sub>6.1, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins.<ref name="entrez" />
| summary_text = [[Potassium channels]] are present in most [[mammalian]] cells, where they participate in a wide range of physiologic responses. K<sub>ir</sub>6.1 is an integral [[membrane protein]] and inward-rectifier type potassium channel. K<sub>ir</sub>6.1, which has a greater tendency to allow [[potassium]] to flow into a cell rather than out of a cell, is controlled by [[G-proteins]].<ref name="entrez" />
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*{{cite journal  | author=Surah-Narwal S |title=Block of human aorta Kir6.1 by the vascular KATP channel inhibitor U37883A |journal=Br. J. Pharmacol. |volume=128 |issue= 3 |pages= 667–672 |year= 1999 |pmid= 10516647 |doi= 10.1038/sj.bjp.0702862  | pmc=1571700  |name-list-format=vanc| author2=Xu SZ  | author3=McHugh D  | display-authors=3  | last4=McDonald  | first4=R L  | last5=Hough  | first5=E  | last6=Cheong  | first6=A  | last7=Partridge  | first7=C  | last8=Sivaprasadarao  | first8=A  | last9=Beech  | first9=D J }}
*{{cite journal  | author=Surah-Narwal S |title=Block of human aorta Kir6.1 by the vascular KATP channel inhibitor U37883A |journal=Br. J. Pharmacol. |volume=128 |issue= 3 |pages= 667–672 |year= 1999 |pmid= 10516647 |doi= 10.1038/sj.bjp.0702862  | pmc=1571700  |name-list-format=vanc| author2=Xu SZ  | author3=McHugh D  | display-authors=3  | last4=McDonald  | first4=R L  | last5=Hough  | first5=E  | last6=Cheong  | first6=A  | last7=Partridge  | first7=C  | last8=Sivaprasadarao  | first8=A  | last9=Beech  | first9=D J }}
*{{cite journal  |vauthors=Tucker SJ, Ashcroft FM |title=Mapping of the physical interaction between the intracellular domains of an inwardly rectifying potassium channel, Kir6.2 |journal=J. Biol. Chem. |volume=274 |issue= 47 |pages= 33393–33397 |year= 1999 |pmid= 10559219 |doi=10.1074/jbc.274.47.33393  }}
*{{cite journal  |vauthors=Tucker SJ, Ashcroft FM |title=Mapping of the physical interaction between the intracellular domains of an inwardly rectifying potassium channel, Kir6.2 |journal=J. Biol. Chem. |volume=274 |issue= 47 |pages= 33393–33397 |year= 1999 |pmid= 10559219 |doi=10.1074/jbc.274.47.33393  }}
*{{cite journal  | author=Kono Y |title=The properties of the Kir6.1-6.2 tandem channel co-expressed with SUR2A |journal=Pflugers Arch. |volume=440 |issue= 5 |pages= 692–698 |year= 2001 |pmid= 11007308 |doi=10.1007/s004240000315  |name-list-format=vanc| author2=Horie M  | author3=Takano M  | display-authors=3  | last4=Otani  | first4=Hideo  | last5=Xie  | first5=Lai-Hua  | last6=Akao  | first6=M.  | last7=Tsuji  | first7=Keiko  | last8=Sasayama  | first8=Shigetake  }}
*{{cite journal  | author=Kono Y |title=The properties of the Kir6.1-6.2 tandem channel co-expressed with SUR2A |journal=Pflügers Arch. |volume=440 |issue= 5 |pages= 692–698 |year= 2001 |pmid= 11007308 |doi=10.1007/s004240000315  |name-list-format=vanc| author2=Horie M  | author3=Takano M  | display-authors=3  | last4=Otani  | first4=Hideo  | last5=Xie  | first5=Lai-Hua  | last6=Akao  | first6=M.  | last7=Tsuji  | first7=Keiko  | last8=Sasayama  | first8=Shigetake  }}
*{{cite journal  |vauthors=Cui Y, Giblin JP, Clapp LH, Tinker A |title=A mechanism for ATP-sensitive potassium channel diversity: Functional coassembly of two pore-forming subunits |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=98 |issue= 2 |pages= 729–734 |year= 2001 |pmid= 11136227 |doi= 10.1073/pnas.011370498  | pmc=14656 }}
*{{cite journal  |vauthors=Cui Y, Giblin JP, Clapp LH, Tinker A |title=A mechanism for ATP-sensitive potassium channel diversity: Functional coassembly of two pore-forming subunits |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=98 |issue= 2 |pages= 729–734 |year= 2001 |pmid= 11136227 |doi= 10.1073/pnas.011370498  | pmc=14656 }}
*{{cite journal  | author=Liu Y |title=Pharmacological comparison of native mitochondrial K(ATP) channels with molecularly defined surface K(ATP) channels |journal=Mol. Pharmacol. |volume=59 |issue= 2 |pages= 225–30 |year= 2001 |pmid= 11160857 |doi=  |name-list-format=vanc| author2=Ren G  | author3=O'Rourke B  | display-authors=3  | last4=Marbán  | first4=E  | last5=Seharaseyon  | first5=J  }}
*{{cite journal  | author=Liu Y |title=Pharmacological comparison of native mitochondrial K(ATP) channels with molecularly defined surface K(ATP) channels |journal=Mol. Pharmacol. |volume=59 |issue= 2 |pages= 225–30 |year= 2001 |pmid= 11160857 |doi=  |name-list-format=vanc| author2=Ren G  | author3=O'Rourke B  | display-authors=3  | last4=Marbán  | first4=E  | last5=Seharaseyon  | first5=J  }}

Latest revision as of 16:03, 29 June 2018

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Identifiers
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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
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RefSeq (mRNA)

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RefSeq (protein)

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Potassium inwardly-rectifying channel, subfamily J, member 8, also known as KCNJ8, is a human gene encoding the Kir6.1 protein.[1] A mutation in KCNJ8 has been associated with cardiac arrest in the early repolarization syndrome.

Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. Kir6.1 is an integral membrane protein and inward-rectifier type potassium channel. Kir6.1, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins.[1]

See also

References

  1. 1.0 1.1 "Entrez Gene: KCNJ8 potassium inwardly-rectifying channel, subfamily J, member 8".

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.