KCNN2

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.[3] KCNN2 is an ion channel protein also known as KCa2.2.[4]

KCNN2
Identifiers
AliasesKCNN2, KCa2.2, SK2, SKCA2, SKCa 2, hSK2, potassium calcium-activated channel subfamily N member 2
External IDsOMIM: 605879 HomoloGene: 23150 GeneCards: KCNN2
Gene location (Human)
Chr.Chromosome 5 (human)[1]
Band5q22.3Start114,055,926 bp[1]
End114,496,500 bp[1]
RNA expression pattern
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez

3781

n/a

Ensembl

ENSG00000080709

n/a

UniProt

Q9H2S1

n/a

RefSeq (mRNA)

NM_001278204
NM_021614
NM_170775
NM_001372233

n/a

RefSeq (protein)

NP_001265133
NP_067627
NP_740721
NP_001359162

n/a

Location (UCSC)Chr 5: 114.06 – 114.5 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

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.[4]

In a 2009 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.[5] In a 2015 study, it was found that UBE3A, the protein maternally deleted in Angelman syndrome, marks KCNN2 for degradation in the hippocampus, and that UBE3A deficiency is associated with an increase in KCNN2 levels. KCNN2 operates through a negative feedback loop to reduce glutamatergic NMDA receptor activation when it itself is activated by that same receptor. Angelman syndrome therefore leads to a reduction in glutamatergic NMDA receptor activation, which impairs long-term potentiation of hippocampal neurons and thus fear conditioning.[6]

See also

References

  1. GRCh38: Ensembl release 89: ENSG00000080709 - Ensembl, May 2017
  2. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. 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. S2CID 8290401.
  4. "Entrez Gene: KCNN2 potassium intermediate/small conductance calcium-activated channel, subfamily N, member 2".
  5. 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.
  6. Sun, Jiandong; Zhu, Guoqi; Liu, Yan; Standley, Steve; Ji, Angela; Tunuguntla, Rashmi; Wang, Yubin; Claus, Chad; Luo, Yun; Baudry, Michel; Bi, Xiaoning (2015-07-21). "UBE3A Regulates Synaptic Plasticity and Learning and Memory by Controlling SK2 Channel Endocytosis". Cell Reports. 12 (3): 449–461. doi:10.1016/j.celrep.2015.06.023. ISSN 2211-1247. PMC 4520703. PMID 26166566.

Further reading

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


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