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Gene Review

Kcnn2  -  potassium intermediate/small conductance...

Mus musculus

Synonyms: KCa2.2, SK2, SKCA2, SKCa 2, SKCa2, ...
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High impact information on Kcnn2

  • The SK2 subtype of small conductance Ca2+-activated K+ channels is widely distributed throughout the central nervous system and modulates neuronal excitability by contributing to the afterhyperpolarization that follows an action potential [1].
  • Endothelial NOS was increased but SK2, SK3 and connexin (Cx) 37 mRNA expressions were significantly (P<0.05) decreased in the SMA from STZ-treated apoE-deficient mice compared to the CIT-treated controls [2].
  • The microvasculature of STZ-induced apoE-deficient mice developed endothelial dysfunction, which may be linked to a decrease in the contribution of the EDHF component due to a decrease in SK2 and 3 and Cx 37 expression [2].
  • We conclude that SK2 channels in substantia nigra pars reticulata neurons are activated by Ca2+ influx through at least two types of Ca2+ channels in the membrane and by ryanodine receptor-mediated Ca2+ release from intracellular stores [3].
  • In HEK-293 cells cotransfected with cochlear SK2 plus alpha9/alpha10 receptors, acetylcholine induced an inward current followed by a robust outward current [4].

Biological context of Kcnn2

  • Consistent with this, SK2 overexpression reduced long-term potentiation after high-frequency stimulation compared with WT littermates and severely impaired learning in both hippocampus- and amygdala-dependent tasks [5].

Anatomical context of Kcnn2

  • To determine the specific influence of SK2 channels on hippocampal synaptic plasticity, learning, and memory, we used gene targeting through homologous recombination in embryonic stem cells to generate transgenic mice that overexpress SK2 subunits by 10-fold (SK2+/T) [5].
  • Here we report the cloning, characterization, and expression of a complete SK2 cDNA from the mouse cochlea [4].
  • The results indicate that SK2 and the alpha9/alpha10 acetylcholine receptors are sufficient to partly recapitulate the native hair cell efferent synaptic response [4].
  • Human cultured cell lines transfected with SK2 yielded Ca(2+)-sensitive K+ current that was blocked by dequalinium chloride and apamin, known blockers of SK channels [4].
  • Xenopus oocytes injected with SK2 in vitro transcribed RNA, under conditions where only outward K+ currents could be recorded, expressed an outward current that was sensitive to EGTA, dequalinium chloride, and apamin [4].

Associations of Kcnn2 with chemical compounds

  • Neurons in substantia nigra pars reticulata express the messenger RNA for SK2 but not for SK3 subunits that form small-conductance, Ca2+-dependent K+ channels in dopamine neurons [3].

Analytical, diagnostic and therapeutic context of Kcnn2


  1. A novel isoform of SK2 assembles with other SK subunits in mouse brain. Strassmaier, T., Bond, C.T., Sailer, C.A., Knaus, H.G., Maylie, J., Adelman, J.P. J. Biol. Chem. (2005) [Pubmed]
  2. Endothelial dysfunction in the streptozotocin-induced diabetic apoE-deficient mouse. Ding, H., Hashem, M., Wiehler, W.B., Lau, W., Martin, J., Reid, J., Triggle, C. Br. J. Pharmacol. (2005) [Pubmed]
  3. Two pathways for the activation of small-conductance potassium channels in neurons of substantia nigra pars reticulata. Yanovsky, Y., Zhang, W., Misgeld, U. Neuroscience (2005) [Pubmed]
  4. Cloning and expression of a small-conductance Ca(2+)-activated K+ channel from the mouse cochlea: coexpression with alpha9/alpha10 acetylcholine receptors. Nie, L., Song, H., Chen, M.F., Chiamvimonvat, N., Beisel, K.W., Yamoah, E.N., Vázquez, A.E. J. Neurophysiol. (2004) [Pubmed]
  5. Small-conductance Ca2+-activated K+ channel type 2 (SK2) modulates hippocampal learning, memory, and synaptic plasticity. Hammond, R.S., Bond, C.T., Strassmaier, T., Ngo-Anh, T.J., Adelman, J.P., Maylie, J., Stackman, R.W. J. Neurosci. (2006) [Pubmed]
  6. Small-conductance calcium-activated K+ channels are expressed in pancreatic islets and regulate glucose responses. Tamarina, N.A., Wang, Y., Mariotto, L., Kuznetsov, A., Bond, C., Adelman, J., Philipson, L.H. Diabetes (2003) [Pubmed]
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