The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Kcna1  -  potassium voltage-gated channel, shaker...

Mus musculus

Synonyms: AI840627, Kca1-1, Kv1.1, MBK1, MKI, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Kcna1


Psychiatry related information on Kcna1


High impact information on Kcna1

  • Currents expressed in naive CD4(+) lymphocytes are consistent with Kv1.1, Kv1.2, Kv1.3, and Kv1 [9].
  • The contactin mutation does not affect sodium channel clustering at the nodes of Ranvier but alters the location of the Shaker-type Kv1.1 and Kv1.2 potassium channels [10].
  • Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs [11].
  • We recently have reported that suppression of the slowly inactivating component of the outward current, Islow, in ventricular myocytes of transgenic mice (long QT mice) overexpressing the N-terminal fragment and S1 segment of Kv1.1 resulted in a significant prolongation of action potential duration and the QT interval [12].
  • At the cellular level, we propose that Kv1.1 deletion enhances excitability of the basket cells by selectively enhancing the likelihood of action potential propagation past axonal branch points [6].

Chemical compound and disease context of Kcna1


Biological context of Kcna1

  • There were no significant differences in intrinsic membrane properties and action potential shape between Kcna1-null and wild-type mice, consistent with previous findings in hippocampal slice recordings [15].
  • When extracellular potassium was elevated and excitatory synaptic transmission was blocked, antidromic activation or short pulses of intracellular depolarizing current evoked voltage-dependent bursts of action potentials in the majority of cells recorded in Kcna1 null slices, but only single spikes in control slices [16].
  • Two neurological mutants deafwaddler (dfw) and opisthotonos (opt) and a cluster of three Shaker-like potassium (K) channel genes Kcna1, Kcna5, and Kcna6 were all independently mapped to distal mouse chromosome six (Chr 6) [17].
  • Together these results suggest (1) heteromeric assembly of Shaker-like channels is cotranslational, and (2) N207 glycosylation of Kv1.1 occurs but is not required for subunit assembly, transport, or function [18].
  • We show that mceph/mceph mice have disturbed brain electrophysiology and experience recurrent behavioural seizures, in agreement with the abnormal electrical brain activity found in Shaker mutants [1].

Anatomical context of Kcna1

  • METHODS: Intracellular recordings were obtained from CA3 pyramidal cells in hippocampal slices prepared from Kcna1-null and control littermates [16].
  • Evidence of altered inhibition in layer V pyramidal neurons from neocortex of Kcna1-null mice [15].
  • The voltage-gated potassium (Kv) channel subunit Kv1.1, encoded by the Kcna1 gene, is expressed strongly in the ventral cochlear nucleus (VCN) and the medial nucleus of the trapezoid body (MNTB) of the auditory pathway [19].
  • Localization of Kv1.1 and Kv1.2, two K channel proteins, to synaptic terminals, somata, and dendrites in the mouse brain [20].
  • Pharmacological characterization of five cloned voltage-gated K+ channels, types Kv1.1, 1.2, 1.3, 1.5, and 3.1, stably expressed in mammalian cell lines [21].

Associations of Kcna1 with chemical compounds

  • Our results show that a voltage-gated sodium channel (Scn1b) and a voltage-gated potassium channel (Kcna1) are differentially expressed in AGS and PTZ-induced epilepsy models as well as in QYS-treated animals [22].
  • Gal(beta1-3)GalNAc binding sites did not have an obligatory co-localization with voltage-gated sodium channels or the potassium ion channels Kv1.1 and Kv1.5 and are thus not likely carried by these ion channels [23].
  • To gain insight into the pathogenesis of these neuropathies, we examined the distribution of GM1 ganglioside and Gal(beta1-3)GalNAc moieties in nerve fibres and their relationship to voltage-gated sodium and potassium (Kv1.1, 1.5) channels at the nodes of Ranvier in peripheral nerves from human, rat and dystrophic mice [23].
  • We demonstrated that overexpression of a cRNA encoding a truncated potassium channel polypeptide that contains the NH2 terminus and the first transmembrane segment (Kv1.1N206Tag) abolished the expression of Kv1.1 and Kv1.5 outward currents in Xenopus oocytes (Babila, T., Moscucci, A., Wang, H., Weaver, F. E. & Koren, G. (1994) Neuron 12, 615-626) [3].
  • Overexpression of a dominant-negative truncated Kv1.1 (Kv1DN) polypeptide in the mouse heart resulted in marked attenuation of a 4-aminopyridine (4-AP)-sensitive current, I(K,slow1) [24].

Regulatory relationships of Kcna1

  • Thus, Kv1.5 encodes the 4-AP-sensitive component of I(K,slow) in the mouse ventricle and confers sensitivity to 4-AP-induced prolongation of APD and QTC: Compensatory upregulation of Kv2.1 may explain the phenotypic differences between SWAP mice and the previously described transgenic mice expressing a truncated dominant-negative Kv1.1 construct [25].
  • When Kv1.1 was expressed as a heterotetrameric complex with Kv1.5, block by DTX-K dominated, indicating that one or more subunits of Kv1.1 rendered the heterotetrameric channel sensitive to DTX-K [26].

Other interactions of Kcna1

  • Of particular interest is the stark contrast between high level expression of Kv1.1 and very low level expression of Kv3.1 in the octopus cell area of the cochlear nucleus and in the lateral superior olivary nucleus [27].
  • The non-Shaker Kv2.1 channel did not assemble with Kv1.1 or Kv1 [18].
  • This property of CA3 neurons, seen particularly when tissue conditions become abnormal (e.g., elevated extracellular potassium), helps to explain the high seizure susceptibility of Kcna1-null mice [16].
  • However, in contrast to the commonly demonstrated epilepsy-induced neurodegeneration, we find that the mceph mutation leads to seizures with a concomitant increase in brain size, without overt neural atrophy [1].
  • These data suggest that the IGF system has an important role in the excessive growth of the mceph/mceph brains [28].

Analytical, diagnostic and therapeutic context of Kcna1


  1. Truncation of the Shaker-like voltage-gated potassium channel, Kv1.1, causes megencephaly. Petersson, S., Persson, A.S., Johansen, J.E., Ingvar, M., Nilsson, J., Klement, G., Arhem, P., Schalling, M., Lavebratt, C. Eur. J. Neurosci. (2003) [Pubmed]
  2. Neuromyotonia and limbic encephalitis sera target mature Shaker-type K+ channels: subunit specificity correlates with clinical manifestations. Kleopa, K.A., Elman, L.B., Lang, B., Vincent, A., Scherer, S.S. Brain (2006) [Pubmed]
  3. A cellular model for long QT syndrome. Trapping of heteromultimeric complexes consisting of truncated Kv1.1 potassium channel polypeptides and native Kv1.4 and Kv1.5 channels in the endoplasmic reticulum. Folco, E., Mathur, R., Mori, Y., Buckett, P., Koren, G. J. Biol. Chem. (1997) [Pubmed]
  4. Characterization of mice with a combined suppression of I(to) and I(K,slow). Brunner, M., Guo, W., Mitchell, G.F., Buckett, P.D., Nerbonne, J.M., Koren, G. Am. J. Physiol. Heart Circ. Physiol. (2001) [Pubmed]
  5. Involvement of kv1 potassium channels in spreading acidification and depression in the cerebellar cortex. Chen, G., Gao, W., Reinert, K.C., Popa, L.S., Hendrix, C.M., Ross, M.E., Ebner, T.J. J. Neurophysiol. (2005) [Pubmed]
  6. Specific alteration of spontaneous GABAergic inhibition in cerebellar purkinje cells in mice lacking the potassium channel Kv1. 1. Zhang, C.L., Messing, A., Chiu, S.Y. J. Neurosci. (1999) [Pubmed]
  7. Differential effects of acute and chronic electroconvulsive shock on the abundance of messenger RNAs for voltage-dependent potassium channel subunits in the rat brain. Pei, Q., Burnet, P.W., Grahame-Smith, D.G., Zetterström, T.S. Neuroscience (1997) [Pubmed]
  8. Kv1.1 channel antisense attenuates learning and modulation of dentate polysialylated NCAM. Gratacós, E., Ghelardini, C., Gherardini, L.M., Galeotti, N., Murphy, K.J., Bartolini, A., Regan, C.M. Neuroreport (1998) [Pubmed]
  9. Modulation of Kv channel expression and function by TCR and costimulatory signals during peripheral CD4(+) lymphocyte differentiation. Liu, Q.H., Fleischmann, B.K., Hondowicz, B., Maier, C.C., Turka, L.A., Yui, K., Kotlikoff, M.I., Wells, A.D., Freedman, B.D. J. Exp. Med. (2002) [Pubmed]
  10. Contactin orchestrates assembly of the septate-like junctions at the paranode in myelinated peripheral nerve. Boyle, M.E., Berglund, E.O., Murai, K.K., Weber, L., Peles, E., Ranscht, B. Neuron (2001) [Pubmed]
  11. Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes. Archer, S.L., Souil, E., Dinh-Xuan, A.T., Schremmer, B., Mercier, J.C., El Yaagoubi, A., Nguyen-Huu, L., Reeve, H.L., Hampl, V. J. Clin. Invest. (1998) [Pubmed]
  12. Characterization of a slowly inactivating outward current in adult mouse ventricular myocytes. Zhou, J., Jeron, A., London, B., Han, X., Koren, G. Circ. Res. (1998) [Pubmed]
  13. Kv1.1 deletion augments the afferent hypoxic chemosensory pathway and respiration. Kline, D.D., Buniel, M.C., Glazebrook, P., Peng, Y.J., Ramirez-Navarro, A., Prabhakar, N.R., Kunze, D.L. J. Neurosci. (2005) [Pubmed]
  14. Kv1.1 channels of dorsal root ganglion neurons are inhibited by n-butyl-p-aminobenzoate, a promising anesthetic for the treatment of chronic pain. Beekwilder, J.P., O'Leary, M.E., van den Broek, L.P., van Kempen, G.T., Ypey, D.L., van den Berg, R.J. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  15. Evidence of altered inhibition in layer V pyramidal neurons from neocortex of Kcna1-null mice. van Brederode, J.F., Rho, J.M., Cerne, R., Tempel, B.L., Spain, W.J. Neuroscience (2001) [Pubmed]
  16. Hyperexcitability of CA3 pyramidal cells in mice lacking the potassium channel subunit Kv1.1. Lopantsev, V., Tempel, B.L., Schwartzkroin, P.A. Epilepsia (2003) [Pubmed]
  17. Molecular genetic analysis of distal mouse chromosome 6 defines gene order and positions of the deafwaddler and opisthotonos mutations. Street, V.A., Robinson, L.C., Erford, S.K., Tempel, B.L. Genomics (1995) [Pubmed]
  18. The brain Kv1.1 potassium channel: in vitro and in vivo studies on subunit assembly and posttranslational processing. Deal, K.K., Lovinger, D.M., Tamkun, M.M. J. Neurosci. (1994) [Pubmed]
  19. Decreased temporal precision of auditory signaling in Kcna1-null mice: an electrophysiological study in vivo. Kopp-Scheinpflug, C., Fuchs, K., Lippe, W.R., Tempel, B.L., Rübsamen, R. J. Neurosci. (2003) [Pubmed]
  20. Localization of Kv1.1 and Kv1.2, two K channel proteins, to synaptic terminals, somata, and dendrites in the mouse brain. Wang, H., Kunkel, D.D., Schwartzkroin, P.A., Tempel, B.L. J. Neurosci. (1994) [Pubmed]
  21. Pharmacological characterization of five cloned voltage-gated K+ channels, types Kv1.1, 1.2, 1.3, 1.5, and 3.1, stably expressed in mammalian cell lines. Grissmer, S., Nguyen, A.N., Aiyar, J., Hanson, D.C., Mather, R.J., Gutman, G.A., Karmilowicz, M.J., Auperin, D.D., Chandy, K.G. Mol. Pharmacol. (1994) [Pubmed]
  22. Involvement of Scn1b and Kcna1 ion channels in audiogenic seizures and PTZ-induced epilepsy. Li, X., Yang, Q., Kuang, H., Jiang, N., Hu, Y. Epilepsy Res. (2005) [Pubmed]
  23. The distribution of ganglioside-like moieties in peripheral nerves. Sheikh, K.A., Deerinck, T.J., Ellisman, M.H., Griffin, J.W. Brain (1999) [Pubmed]
  24. Long-term restitution of 4-aminopyridine-sensitive currents in Kv1DN ventricular myocytes using adeno-associated virus-mediated delivery of Kv1.5. Kodirov, S.A., Brunner, M., Busconi, L., Koren, G. FEBS Lett. (2003) [Pubmed]
  25. Targeted replacement of KV1.5 in the mouse leads to loss of the 4-aminopyridine-sensitive component of I(K,slow) and resistance to drug-induced qt prolongation. London, B., Guo, W., Pan Xh, n.u.l.l., Lee, J.S., Shusterman, V., Rocco, C.J., Logothetis, D.A., Nerbonne, J.M., Hill, J.A. Circ. Res. (2001) [Pubmed]
  26. Functional and molecular expression of a voltage-dependent K(+) channel (Kv1.1) in interstitial cells of Cajal. Hatton, W.J., Mason, H.S., Carl, A., Doherty, P., Latten, M.J., Kenyon, J.L., Sanders, K.M., Horowitz, B. J. Physiol. (Lond.) (2001) [Pubmed]
  27. Differential expression of voltage-gated potassium channel genes in auditory nuclei of the mouse brainstem. Grigg, J.J., Brew, H.M., Tempel, B.L. Hear. Res. (2000) [Pubmed]
  28. The megencephaly mouse has disturbances in the insulin-like growth factor (IGF) system. Petersson, S., Sandberg Nordqvist, A., Schalling, M., Lavebratt, C. Brain Res. Mol. Brain Res. (1999) [Pubmed]
  29. Hyperexcitability and reduced low threshold potassium currents in auditory neurons of mice lacking the channel subunit Kv1.1. Brew, H.M., Hallows, J.L., Tempel, B.L. J. Physiol. (Lond.) (2003) [Pubmed]
  30. A truncated Kv1.1 protein in the brain of the megencephaly mouse: expression and interaction. Persson, A.S., Klement, G., Almgren, M., Sahlholm, K., Nilsson, J., Petersson, S., Arhem, P., Schalling, M., Lavebratt, C. BMC neuroscience [electronic resource]. (2005) [Pubmed]
  31. Expression of Kv1.1, a Shaker-like potassium channel, is temporally regulated in embryonic neurons and glia. Hallows, J.L., Tempel, B.L. J. Neurosci. (1998) [Pubmed]
  32. The Shaker-like potassium channels of the mouse rod bipolar cell and their contributions to the membrane current. Klumpp, D.J., Song, E.J., Ito, S., Sheng, M.H., Jan, L.Y., Pinto, L.H. J. Neurosci. (1995) [Pubmed]
WikiGenes - Universities