KCNN2

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External IDsGeneCards: [1]
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SpeciesHumanMouse
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Potassium intermediate/small conductance calcium-activated channel, subfamily N, member 2, also known as KCNN2, is a protein which in humans is encoded by the KCNN2 gene.[1] KCNN2 is an ion channel protein also known as KCa2.2.[2]

Function

Action potentials in vertebrate neurons are followed by an afterhyperpolarization (AHP) that may persist for several seconds and may have profound consequences for the firing pattern of the neuron. Each component of the AHP is kinetically distinct and is mediated by different calcium-activated potassium channels. The KCa2.2 protein is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP. KCa2.2 is an integral membrane protein that forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. This protein is a member of the calcium-activated potassium channel family. Two transcript variants encoding different isoforms have been found for the KCNN2 gene.[2]

In a study SK2 (KCNN2) potassium channel was overexpressed in the basolateral amygdala using a herpes simplex viral system. This reduced anxiety and stress-induced corticosterone secretion at a systemic level. SK2 overexpression also reduced dendritic arborization of the amygdala neurons.[3]

See also

References

  1. Wei AD, Gutman GA, Aldrich R, Chandy KG, Grissmer S, Wulff H (December 2005). "International Union of Pharmacology. LII. Nomenclature and molecular relationships of calcium-activated potassium channels". Pharmacol. Rev. 57 (4): 463–72. doi:10.1124/pr.57.4.9. PMID 16382103.
  2. 2.0 2.1 "Entrez Gene: KCNN2 potassium intermediate/small conductance calcium-activated channel, subfamily N, member 2".
  3. Mitra R, Ferguson D, Sapolsky RM (February 2009). "SK2 potassium channel over-expression in basolateral amygdala reduces anxiety, stress-induced corticosterone and dendritic arborization". Mol. Psychiatry. 14 (9): 847–55, 827. doi:10.1038/mp.2009.9. PMC 2763614. PMID 19204724.

Further reading

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



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