KCND3

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Potassium voltage-gated channel, Shal-related subfamily, member 3

PDB rendering based on 1s1g.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols KCND3 ; KCND3L; KCND3S; KSHIVB; KV4.3
External IDs OMIM605411 MGI1928743 HomoloGene21036 IUPHAR: Kv4.3 ChEMBL: 1964 GeneCards: KCND3 Gene
RNA expression pattern
PBB GE KCND3 211827 s at tn.png
PBB GE KCND3 211301 at tn.png
PBB GE KCND3 215014 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 3752 56543
Ensembl ENSG00000171385 ENSMUSG00000040896
UniProt Q9UK17 Q9Z0V1
RefSeq (mRNA) NM_004980 NM_001039347
RefSeq (protein) NP_004971 NP_001034436
Location (UCSC) Chr 1:
112.31 – 112.53 Mb
Chr 3:
105.45 – 105.67 Mb
PubMed search [1] [2]

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.123 It contributes to the cardiac transient outward potassium current (Ito1), the main contributing current to the repolarizing phase 1 of the cardiac action potential.4

Function

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.3

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

References

  1. ^ 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. 
  2. ^ 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. 
  3. ^ a b "Entrez Gene: KCND3 potassium voltage-gated channel, Shal-related subfamily, member 3". 
  4. ^ 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.








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