KCNJ5

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

G protein-activated inward rectifier potassium channel 4 (GIRK-4) is a protein that in humans is encoded by the KCNJ5 gene and is a type of G protein-gated ion channel.[5][6]

AliasesKCNJ5, CIR, GIRK4, KATP1, KIR3.4, LQT13, potassium voltage-gated channel subfamily J member 5, potassium inwardly rectifying channel subfamily J member 5
End128,921,163 bp[1]
Quick facts Identifiers, Aliases ...
KCNJ5
Identifiers
AliasesKCNJ5, CIR, GIRK4, KATP1, KIR3.4, LQT13, potassium voltage-gated channel subfamily J member 5, potassium inwardly rectifying channel subfamily J member 5
External IDsOMIM: 600734; MGI: 104755; HomoloGene: 20248; GeneCards: KCNJ5; OMA:KCNJ5 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000890
NM_001354169

NM_010605

RefSeq (protein)

NP_000881
NP_001341098

NP_034735

Location (UCSC)Chr 11: 128.89 – 128.92 MbChr 9: 32.23 – 32.26 Mb
PubMed search[3][4]
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Function

Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and an inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins. It may associate with other G-protein-activated potassium channel subunits to form a heterotetrameric pore-forming complex.[6]

In humans KCNJ5 is mainly expressed in the adrenal gland and pituitary, although it is also detected at low levels in the pancreas, spleen, lung, heart and brain.[7] Consistent with this expression pattern, mutations in KCNJ5/Kir3.4 can cause familial hyperaldosteronism type III and a type of long QT syndrome.[8]

Interactions

KCNJ5 has been shown to interact with KCNJ3.[9][10]

See also

References

Further reading

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