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Protein KCND3 PDB 1s1g.png
Available structures
PDBOrtholog search: PDBe RCSB
AliasesKCND3, KCND3L, KCND3S, KSHIVB, KV4.3, SCA19, SCA22, BRGDA9, potassium voltage-gated channel subfamily D member 3
External IDsOMIM: 605411 MGI: 1928743 HomoloGene: 21036 GeneCards: KCND3
Gene location (Human)
Chromosome 1 (human)
Chr.Chromosome 1 (human)[1]
Chromosome 1 (human)
Genomic location for KCND3
Genomic location for KCND3
Band1p13.2Start111,770,662 bp[1]
End111,989,155 bp[1]
RNA expression pattern
PBB GE KCND3 211301 at fs.png

PBB GE KCND3 215014 at fs.png

PBB GE KCND3 211827 s at fs.png
More reference expression data
RefSeq (mRNA)



RefSeq (protein)



Location (UCSC)Chr 1: 111.77 – 111.99 MbChr 3: 105.45 – 105.67 Mb
PubMed search[3][4]
View/Edit HumanView/Edit Mouse

Potassium voltage-gated channel subfamily D member 3 also known as Kv4.3 is a protein that in humans is encoded by the KCND3 gene.[5][6][7] It contributes to the cardiac transient outward potassium current (Ito1), the main contributing current to the repolarizing phase 1 of the cardiac action potential.[8]


Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes – shaker, shaw, shab, and shal – have been identified in Drosophila, and each has been shown to have human homolog(s).

Kv4.3 is a member of the potassium channel, voltage-gated, shal-related subfamily, members of which form voltage-activated A-type potassium ion channels and are prominent in the repolarization phase of the action potential. This member includes two isoforms with different sizes, which are encoded by alternatively spliced transcript variants of this gene.[7]

Clinical significance

Gain of function is believed to cause Brugada Syndrome although only indirectly shown by mutations in the beta subunit KCNE3 which causes gain of function of Kv4.3.

See also


  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000171385 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000040896 - Ensembl, 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. ^ Postma AV, Bezzina CR, de Vries JF, Wilde AA, Moorman AF, Mannens MM (Aug 2000). "Genomic organisation and chromosomal localisation of two members of the KCND ion channel family, KCND2 and KCND3". Hum Genet. 106 (6): 614–9. doi:10.1007/s004390050033. PMID 10942109.
  6. ^ Gutman GA, Chandy KG, Grissmer S, Lazdunski M, McKinnon D, Pardo LA, Robertson GA, Rudy B, Sanguinetti MC, Stuhmer W, Wang X (Dec 2005). "International Union of Pharmacology. LIII. Nomenclature and molecular relationships of voltage-gated potassium channels". Pharmacol Rev. 57 (4): 473–508. doi:10.1124/pr.57.4.10. PMID 16382104.
  7. ^ a b "Entrez Gene: KCND3 potassium voltage-gated channel, Shal-related subfamily, member 3".
  8. ^ Oudit GY, Kassiri Z, Sah R, Ramirez RJ, Zobel C, Backx PH (May 2001). "The molecular physiology of the cardiac transient outward potassium current (I(to)) in normal and diseased myocardium". J. Mol. Cell. Cardiol. 33 (5): 851–72. doi:10.1006/jmcc.2001.1376. PMID 11343410.

Further reading

External links

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