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Gene Review

KCNB2  -  potassium channel, voltage gated Shab...

Homo sapiens

Synonyms: Kv2.2, Potassium voltage-gated channel subfamily B member 2, Voltage-gated potassium channel subunit Kv2.2
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High impact information on KCNB2

  • 2. Surprisingly, many myocytes contain transcripts for Kv1.3, Kv2.2, Kv4.1, Kv5.1, and members of the Kv3 family [1].
  • Cell-specific markers were used to show that Kv2.1, Kv3.2, Kv6.2, and Kv9.3 are expressed in beta-cells, that Kv3.1 and Kv6.1 are expressed in alpha-cells, and that Kv2.2 is expressed in delta-cells [2].
  • Present results indicate that Kv8.1 when expressed at low concentrations acts as a modifier of Kv2.1 and Kv2.2 activity, while when expressed at high concentrations in oocytes it completely abolishes Kv2.1, Kv2.2, or Kv3.4 K+ channel activity [3].
  • Target soluble N-ethylmaleimide-sensitive factor attachment protein receptors (t-SNAREs) differently regulate activation and inactivation gating of Kv2.2 and Kv2.1: Implications on pancreatic islet cell Kv channels [4].
  • Here, we characterized the interactions of syntaxin 1A and SNAP-25 with Kv2.2 which is highly homologous to Kv2.1, except for the C-terminus [4].

Biological context of KCNB2

  • Reverse transcription-polymerase chain reaction analysis of potassium channel mRNA in the bipolar neurons revealed that the reduction in the IK current density was caused by Kv2.2 mRNA down-regulation [5].

Anatomical context of KCNB2

  • Injection of Kv2.2 mRNA into Xenopus oocytes resulted in the expression of a slowly activating K+ current (time to half maximum current, 97 +/- 8.6 ms) mediated by 15 pS (symmetrical K+) single channels [6].
  • These data suggest that Kv2.2 may contribute to this current in native GI smooth muscle cells [6].
  • In these cells, Kv8.1 expressed alone remains in intracellular compartments, but it can reach the plasma membrane when it associates with Kv2.2, and it then also forms new types of Kv8.1/Kv2 [3].

Other interactions of KCNB2


Analytical, diagnostic and therapeutic context of KCNB2

  • Northern hybridization analysis performed on RNA prepared from tissues and RT-PCR performed on RNA isolated from dispersed and selected smooth muscle cells demonstrate that Kv2.2 is expressed in smooth muscle cells found in all regions of the canine gastrointestinal (GI) tract and in several vascular tissues [6].
  • Molecular cloning techniques identified the full-length sequence of the rabbit ortholog of the Kv2.2 alpha subunit [7].


  1. In situ hybridization reveals extensive diversity of K+ channel mRNA in isolated ferret cardiac myocytes. Brahmajothi, M.V., Morales, M.J., Liu, S., Rasmusson, R.L., Campbell, D.L., Strauss, H.C. Circ. Res. (1996) [Pubmed]
  2. Expression of voltage-gated potassium channels in human and rhesus pancreatic islets. Yan, L., Figueroa, D.J., Austin, C.P., Liu, Y., Bugianesi, R.M., Slaughter, R.S., Kaczorowski, G.J., Kohler, M.G. Diabetes (2004) [Pubmed]
  3. Modes of regulation of shab K+ channel activity by the Kv8.1 subunit. Salinas, M., de Weille, J., Guillemare, E., Lazdunski, M., Hugnot, J.P. J. Biol. Chem. (1997) [Pubmed]
  4. Target soluble N-ethylmaleimide-sensitive factor attachment protein receptors (t-SNAREs) differently regulate activation and inactivation gating of Kv2.2 and Kv2.1: Implications on pancreatic islet cell Kv channels. Wolf-Goldberg, T., Michaelevski, I., Sheu, L., Gaisano, H.Y., Chikvashvili, D., Lotan, I. Mol. Pharmacol. (2006) [Pubmed]
  5. Transforming growth factor-alpha changes firing properties of developing neocortical GABAergic neurons by down-regulation of voltage-gated potassium currents. Namba, H., Takei, N., Nawa, H. Neuroscience (2003) [Pubmed]
  6. Molecular identification of a component of delayed rectifier current in gastrointestinal smooth muscles. Schmalz, F., Kinsella, J., Koh, S.D., Vogalis, F., Schneider, A., Flynn, E.R., Kenyon, J.L., Horowitz, B. Am. J. Physiol. (1998) [Pubmed]
  7. The Kv2.2 alpha subunit contributes to delayed rectifier K(+) currents in myocytes from rabbit corpus cavernosum. Malysz, J., Farrugia, G., Ou, Y., Szurszewski, J.H., Nehra, A., Gibbons, S.J. J. Androl. (2002) [Pubmed]
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