KCNA5

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KCNA5
Identifiers
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_002234

NM_145983

RefSeq (protein)

NP_002225

NP_666095

Location (UCSC)Chr 12: 5.04 – 5.05 MbChr 6: 126.51 – 126.51 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Potassium voltage-gated channel, shaker-related subfamily, member 5, also known as KCNA5 or Kv1.5, is a protein that in humans is encoded by the KCNA5 gene.[5]

Function

Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. KCNA5 encodes a member of the potassium channel, voltage-gated, shaker-related subfamily. This member contains six membrane-spanning domains with a shaker-type repeat in the fourth segment. It belongs to the delayed rectifier class, the function of which could restore the resting membrane potential of beta cells after depolarization, thereby contributing to the regulation of insulin secretion. This gene is intronless, and the gene is clustered with genes KCNA1 and KCNA6 on chromosome 12.[5] Mutations in this gene have been related to both atrial fibrillation[6] and sudden cardiac death.[7] KCNA5 are also key players in pulmonary vascular function, where they play a role in setting the resting membrane potential and its involvement during hypoxic pulmonary vasoconstriction.

Interactions

KCNA5 has been shown to

Actinin, alpha 2.[8][11]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000130037Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000045534Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b "Entrez Gene: KCNA5 potassium voltage-gated channel, shaker-related subfamily, member 5".
  6. PMID 16772329
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Further reading

External links

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


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