KCNJ3

Jump to navigation Jump to search
The printable version is no longer supported and may have rendering errors. Please update your browser bookmarks and please use the default browser print function instead.
VALUE_ERROR (nil)
Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Potassium inwardly-rectifying channel, subfamily J, member 3, also known as KCNJ3 or Kir3.1, is a human gene.[1]

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 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 and plays an important role in regulating heartbeat. It associates with three other G-protein-activated potassium channels to form a hetero-tetrameric pore-forming complex.[1]

Interactions

KCNJ3 has been shown to interact with KCNJ5.[2][3]

See also

References

  1. 1.0 1.1 "Entrez Gene: KCNJ3 potassium inwardly-rectifying channel, subfamily J, member 3".
  2. Huang, C L; Jan Y N; Jan L Y (Apr 1997). "Binding of the G protein betagamma subunit to multiple regions of G protein-gated inward-rectifying K+ channels". FEBS Lett. NETHERLANDS. 405 (3): 291–8. doi:10.1016/S0014-5793(97)00197-X. ISSN 0014-5793. PMID 9108307.
  3. He, Cheng; Yan Xixin; Zhang Hailin; Mirshahi Tooraj; Jin Taihao; Huang Aijun; Logothetis Diomedes E (Feb 2002). "Identification of critical residues controlling G protein-gated inwardly rectifying K(+) channel activity through interactions with the beta gamma subunits of G proteins". J. Biol. Chem. United States. 277 (8): 6088–96. doi:10.1074/jbc.M104851200. ISSN 0021-9258. PMID 11741896.

Further reading

External links

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