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Kcnc3  -  potassium voltage gated channel, Shaw...

Mus musculus

Synonyms: KSHIIID, KShIIID, Kcr2-3, Kv3.3, Potassium voltage-gated channel subfamily C member 3, ...
 
 
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Disease relevance of Kcnc3

 

Psychiatry related information on Kcnc3

  • The lack of Kv3.1 channel subunits is mainly responsible for the constitutively increased locomotor activity and for sleep loss, whereas the absence of Kv3.3 subunits affects cerebellar function, in particular Purkinje cell discharges and olivocerebellar system properties (McMahon et al. 2004, Eur J Neurosci 19, 3317-3327) [2].
  • In spite of the severe motor impairment, Kv3.1/Kv3.3-deficient mice are hyperactive, show increased exploratory activity, and display no obvious learning or memory deficit [1].
 

High impact information on Kcnc3

 

Biological context of Kcnc3

  • Unlike the vertebrate Shaker-related genes that have intronless coding regions, mouse Kv3.3 is encoded by at least two exons separated by 3 kb of intervening sequence [7].
  • Kv3.3-deficient mice display no overt phenotype (Chan, 1997) [1].
  • The graded penetrance of mutant traits appears to depend on the number of null alleles, suggesting that some of the distinct phenotypic traits visible in the absence of Kv3.1 and Kv3.3 K(+) channels are unrelated and may be caused by localized dysfunction in different brain regions [1].
  • Human Kv3.3/KCNC3 is a Shaw-type potassium channel that has been mapped to chromosome 19q13.3-13 [8].
  • 3 protein is about 93% identical to mouse and rat Kv3.3 in the first 659 amino acids before the C-terminal domains diverge greatly as a result of alternative splicing [8].
 

Anatomical context of Kcnc3

 

Associations of Kcnc3 with chemical compounds

  • Induction of metabotropic glutamate receptor-mediated EPSCs was facilitated, whereas longterm depression was not impaired but rather facilitated in Kv3.1/Kv3.3 double-knockout mice [9].
 

Analytical, diagnostic and therapeutic context of Kcnc3

  • Sequence analysis revealed that it is an alternatively spliced form of the mouse Kv3.3 gene, and that the previously reported Kv3.3 mRNA (Ghanshani et al., 1992) is not expressed in cerebellum [10].

References

  1. Alcohol hypersensitivity, increased locomotion, and spontaneous myoclonus in mice lacking the potassium channels Kv3.1 and Kv3.3. Espinosa, F., McMahon, A., Chan, E., Wang, S., Ho, C.S., Heintz, N., Joho, R.H. J. Neurosci. (2001) [Pubmed]
  2. Behavioral motor dysfunction in Kv3-type potassium channel-deficient mice. Joho, R.H., Street, C., Matsushita, S., Knöpfel, T. Genes Brain Behav. (2006) [Pubmed]
  3. Genomic organization, chromosomal localization, tissue distribution, and biophysical characterization of a novel mammalian Shaker-related voltage-gated potassium channel, Kv1.7. Kalman, K., Nguyen, A., Tseng-Crank, J., Dukes, I.D., Chandy, G., Hustad, C.M., Copeland, N.G., Jenkins, N.A., Mohrenweiser, H., Brandriff, B., Cahalan, M., Gutman, G.A., Chandy, K.G. J. Biol. Chem. (1998) [Pubmed]
  4. Kv3 potassium channels control the duration of different arousal states by distinct stochastic and clock-like mechanisms. Joho, R.H., Marks, G.A., Espinosa, F. Eur. J. Neurosci. (2006) [Pubmed]
  5. Kv3 voltage-gated potassium channels regulate neurotransmitter release from mouse motor nerve terminals. Brooke, R.E., Moores, T.S., Morris, N.P., Parson, S.H., Deuchars, J. Eur. J. Neurosci. (2004) [Pubmed]
  6. Allele-dependent changes of olivocerebellar circuit properties in the absence of the voltage-gated potassium channels Kv3.1 and Kv3.3. McMahon, A., Fowler, S.C., Perney, T.M., Akemann, W., Knöpfel, T., Joho, R.H. Eur. J. Neurosci. (2004) [Pubmed]
  7. Genomic organization, nucleotide sequence, and cellular distribution of a Shaw-related potassium channel gene, Kv3.3, and mapping of Kv3.3 and Kv3.4 to human chromosomes 19 and 1. Ghanshani, S., Pak, M., McPherson, J.D., Strong, M., Dethlefs, B., Wasmuth, J.J., Salkoff, L., Gutman, G.A., Chandy, K.G. Genomics (1992) [Pubmed]
  8. Kv3.3 potassium channels in lens epithelium and corneal endothelium. Rae, J.L., Shepard, A.R. Exp. Eye Res. (2000) [Pubmed]
  9. Motor dysfunction and altered synaptic transmission at the parallel fiber-Purkinje cell synapse in mice lacking potassium channels Kv3.1 and Kv3.3. Matsukawa, H., Wolf, A.M., Matsushita, S., Joho, R.H., Knöpfel, T. J. Neurosci. (2003) [Pubmed]
  10. Kv3.3b: a novel Shaw type potassium channel expressed in terminally differentiated cerebellar Purkinje cells and deep cerebellar nuclei. Goldman-Wohl, D.S., Chan, E., Baird, D., Heintz, N. J. Neurosci. (1994) [Pubmed]
 
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