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potassium voltage-gated channel, Shaw-related subfamily, member 2
Identifiers
Symbols KCNC2; MGC138196
External IDs OMIM176256 MGI96668 HomoloGene71199 IUPHAR: Kv3.2 GeneCards: KCNC2 Gene
Orthologs
Species Human Mouse
Entrez 3747 268345
Ensembl ENSG00000166006 ENSMUSG00000035681
UniProt Q96PR1 P70311
RefSeq (mRNA) NM_153748 NM_001025581
RefSeq (protein) NP_631875 NP_001020752
Location (UCSC) Chr 12:
73.72 - 73.89 Mb
Chr 10:
111.71 - 111.9 Mb
PubMed search [1] [2]

Potassium voltage-gated channel subfamily C member 2 is a protein that in humans is encoded by the KCNC2 gene.[1][2][1] The protein encoded by this gene is a voltage-gated potassium channel subunit.[3]

Contents

Expression pattern

Kv3.1 and Kv3.2 channels are prominently expressed in neurons that fire at high frequency. Kv3.2 channels are prominently expressed in brain (fast-spiking GABAergic interneurons of the neocortex, hippocampus, and caudate nucleus; terminal fields of thalamocortical projections), and in retinal ganglion cells.[4][5][3]

Physiological role

Kv3.1/Kv3.2 conductance is necessary and kinetically optimized for high-frequency action potential generation.[5][6] Sometimes in heteromeric complexes with Kv3.1; important for the high-frequency firing of fast spiking GABAergic interneurons and retinal ganglion cells; and GABA release via regulation of action potential duration in presynaptic terminals.[4][3]

Pharmacological properties

Kv3.2 currents in heterologous systems are highly sensitive to external tetraethylammonium (TEA) or 4-aminopyridine (4-AP) (IC50 values are 0.1 mM for both of the drugs).[5][3] This can be useful in identifying native channels.[5]

Transcript variants

There are four transcript variants of Kv3.2 gene: Kv3.2a, Kv3.2b, Kv3.2c, Kv3.2d. Kv3.2 isoforms differ only in their C-terminal sequence.[7]

References

  1. ^ a b Haas M, Ward DC, Lee J, Roses AD, Clarke V, D'Eustachio P, Lau D, Vega-Saenz de Miera E, Rudy B (Mar 1994). "Localization of Shaw-related K+ channel genes on mouse and human chromosomes". Mamm Genome 4 (12): 711-5. PMID 8111118.  
  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 c d 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. ^ a b Kolodin YO (2008-04-27). "Ionic conductances underlying excitability in tonically firing retinal ganglion cells of adult rat". http://ykolodin.50webs.com. Retrieved 2008-10-20.  
  5. ^ a b c d Rudy B, McBain CJ (September 2001). "Kv3 channels: voltage-gated K+ channels designed for high-frequency repetitive firing". Trends in Neurosciences 24 (9): 517–26. doi:10.1016/S0166-2236(00)01892-0. PMID 11506885.  
  6. ^ Lien CC, Jonas P (March 2003). "Kv3 potassium conductance is necessary and kinetically optimized for high-frequency action potential generation in hippocampal interneurons". The Journal of neuroscience : the official journal of the Society for Neuroscience 23 (6): 2058–68. PMID 12657664. http://www.jneurosci.org/cgi/content/full/23/6/2058.  
  7. ^ Rudy B, Chow A, Lau D, Amarillo Y, Ozaita A, Saganich M, Moreno H, Nadal MS, Hernandez-Pineda R, Hernandez-Cruz A, Erisir A, Leonard C, Vega-Saenz de Miera E (April 1999). "Contributions of Kv3 channels to neuronal excitability". Annals of the New York Academy of Sciences 868: 304–43. doi:10.1111/j.1749-6632.1999.tb11295.x. PMID 10414303.  

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