KCNB1

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Potassium voltage-gated channel, Shab-related subfamily, member 1
Identifiers
Symbols KCNB1 ; DRK1; KV2.1; h-DRK1
External IDs OMIM600397 MGI96666 HomoloGene37988 IUPHAR: Kv2.1 GeneCards: KCNB1 Gene
RNA expression pattern
PBB GE KCNB1 211006 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 3745 16500
Ensembl ENSG00000158445 ENSMUSG00000050556
UniProt Q14721 Q03717
RefSeq (mRNA) NM_004975 NM_008420
RefSeq (protein) NP_004966 NP_032446
Location (UCSC) Chr 20:
47.98 – 48.1 Mb
Chr 2:
167.1 – 167.19 Mb
PubMed search [1] [2]

Potassium voltage-gated channel, Shab-related subfamily, member 1, also known as KCNB1 or Kv2.1, is a protein that, in humans, is encoded by the KCNB1 gene.[1][2][3]

Species and tissue distribution[edit]

Kv2.1 channels are widely expressed in various tissues in mammals, including humans. They are found in cardiomyocytes, skeletal muscles, vascular smooth muscles, placental vasculature, retina, and pancreatic β-cells.

Function[edit]

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, shab-related subfamily. This member is a delayed rectifier potassium channel and its activity is modulated by some other family members.[1]

In mouse cardiomyocytes, Kv2.1 channel is the molecular substrate of major repolarization current IK-slow2. Transgenic mice, expressing a dominant-negative isoform of Kv2.1, exhibit markedly prolonged action potentials and demonstrate arrhythmia. In mammalian CNS neurons, Kv2.1 is a predominant delayed rectifier K+ current that regulates neuronal excitability, action potential duration, and tonic spiking.[4] In Drosophila photoreceptor cells, the Kv2 channel is the key component of light-induced membrane voltage response. Genetic abolition of this current dramatically decreases photoreceptor information capacity.

Interactions[edit]

KCNB1 has been shown to interact with:

See also[edit]

References[edit]

  1. ^ a b "Entrez Gene: KCNB1 potassium voltage-gated channel, Shab-related subfamily, member 1". 
  2. ^ Melis R, Stauffer D, Zhao X, Zhu XL, Albrecht B, Pongs O, Brothman A, Leppert M (January 1995). "Physical and genetic localization of a Shab subfamily potassium channel (KCNB1) gene to chromosomal region 20q13.2". Genomics 25 (1): 285–7. doi:10.1016/0888-7543(95)80138-C. PMID 7774931. 
  3. ^ Gutman GA, Chandy KG, Grissmer S, Lazdunski M, McKinnon D, Pardo LA, Robertson GA, Rudy B, Sanguinetti MC, Stühmer 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. 
  4. ^ Murakoshi, H; Trimmer JS (March 1999). "Identification of the Kv2.1 K+ channel as a major component of the delayed rectifier K+ current in rat hippocampal neurons.". J Neurosci. 19 (5): 1728–35. PMID 10024359. 
  5. ^ Ottschytsch N, Raes A, Van Hoorick D, Snyders DJ (June 2002). "Obligatory heterotetramerization of three previously uncharacterized Kv channel alpha-subunits identified in the human genome". Proc. Natl. Acad. Sci. U.S.A. 99 (12): 7986–91. doi:10.1073/pnas.122617999. PMC 123007. PMID 12060745. 
  6. ^ Peretz A, Gil-Henn H, Sobko A, Shinder V, Attali B, Elson A (August 2000). "Hypomyelination and increased activity of voltage-gated K(+) channels in mice lacking protein tyrosine phosphatase epsilon". EMBO J. 19 (15): 4036–45. doi:10.1093/emboj/19.15.4036. PMC 306594. PMID 10921884. 

Further reading[edit]

External links[edit]

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