Potassium voltage-gated channel subfamily D member 2 is a protein that in humans is encoded by the KCND2 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]

KCND2
Identifiers
AliasesKCND2, KV4.2, RK5, potassium voltage-gated channel subfamily D member 2
External IDsOMIM: 605410; MGI: 102663; HomoloGene: 40828; GeneCards: KCND2; OMA:KCND2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_012281

NM_019697

RefSeq (protein)

NP_036413

NP_062671

Location (UCSC)Chr 7: 120.27 – 120.75 MbChr 6: 21.22 – 21.73 Mb
PubMed search[3][4]
Wikidata
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Description

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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). This gene encodes 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 mediates a rapidly inactivating, A-type outward potassium current which is not under the control of the N terminus as it is in Shaker channels.[7]

Interactions

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KCND2 has been shown to interact with FLNC.[9]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000184408Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000060882Ensembl, 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. ^ Zhu XR, Wulf A, Schwarz M, Isbrandt D, Pongs O (December 1999). "Characterization of human Kv4.2 mediating a rapidly-inactivating transient voltage-sensitive K+ current". Receptors Channels. 6 (5): 387–400. PMID 10551270.
  6. ^ Gutman GA, Chandy KG, Grissmer S, Lazdunski M, McKinnon D, Pardo LA, Robertson GA, Rudy B, Sanguinetti MC, Stuhmer W, Wang X (December 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. S2CID 219195192.
  7. ^ a b "Entrez Gene: KCND2 potassium voltage-gated channel, Shal-related subfamily, member 2".
  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): 851–872. doi:10.1006/jmcc.2001.1376. PMID 11343410. S2CID 829154.
  9. ^ Petrecca, K; Miller D M; Shrier A (December 2000). "Localization and enhanced current density of the Kv4.2 potassium channel by interaction with the actin-binding protein filamin". J. Neurosci. 20 (23): 8736–44. doi:10.1523/JNEUROSCI.20-23-08736.2000. PMC 6773047. PMID 11102480.

Further reading

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