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Gene Review

Kcnb1  -  potassium voltage gated channel, Shab...

Mus musculus

Synonyms: Kcr1-1, Kv2.1, Potassium voltage-gated channel subfamily B member 1, Shab, Voltage-gated potassium channel subunit Kv2.1, ...
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Disease relevance of Kcnb1

  • Hypoxia (PO(2)= approximately 30 mm Hg) reversibly inhibited Kv1.2 and Kv2.1 currents only at potentials more positive than 30 mV [1].
  • These findings provide a basis for future studies of (post)transcriptional mechanism(s) down-regulating Kcnb1 expression in a variety of cardiomyopathies and point towards a possible involvement of Kcnb1 in pituitary cell excitability and secretory activity regulated by osmolarity [2].
  • Here we show that a putative Kv2.1 antagonist (C-1) stimulates insulin secretion from MIN6 insulinoma cells in a glucose- and dose-dependent manner while blocking voltage-dependent outward K(+) currents [3].
  • However, attenuation of Kv2.1-encoded currents in Kv1DN mice did not suppress the arrhythmias [4].

High impact information on Kcnb1


Biological context of Kcnb1

  • 2. Whole-cell patch clamp demonstrated the presence of delayed rectifier K+ currents inhibited by tetraethylammonium (TEA) and 4-aminopyridine, with similar Kd values to that of Kv2.1, correlating delayed rectifier gene expression with the K+ currents [8].
  • The protein levels of other Kv alpha subunits, Kv1.2 and Kv2.1, in contrast, are not affected by the expression of the Kv4.2W362F transgene [9].
  • In summary, our data indicate that the spatially restrictive upregulation of Kv2.1-encoded currents underlies the increased dispersion of the repolarization observed in Kv1DN mice [10].
  • Crossbreeding of Kv1DN mice with mice expressing a truncated Kv2.1 polypeptide (Kv2DN) eliminated I(K,slow2) [10].
  • Currents generated by coexpression of Kv2.1 with Kv9.3 alpha subunits were reversibly inhibited by hypoxia in the voltage range of the resting membrane potential (E(M)) of PA VSMCs ( approximately 28% at -40 mV) [1].

Anatomical context of Kcnb1


Associations of Kcnb1 with chemical compounds

  • We found that sustained administration of Ang II decreased Kv currents (IKv) by reducing the expression of Kv2.1 K+ channel subunits [12].
  • In L-cells, 10 to 100 microM OPC-18790 reduced Kv1.4, Kv1.5 and Kv2.1 currents by <30%, whereas quinidine was a more potent blocker (EC50 < 10 microM) and the I(Kr)-specific blocker dofetilide was without effect [14].
  • The insulinotropic effect of acute Kv2.1 inhibition resulted from enhanced membrane depolarization and augmented intracellular Ca(2+) responses to glucose [3].
  • Depletion of cellular cholesterol alters the buoyancy of the Kv2.1 associated rafts and shifts the midpoint of Kv2.1 inactivation by nearly 40 mV without affecting peak current density or channel activation [15].
  • 5. These results can be explained with a model based on an allosteric model of inactivation in Kv2.1 (Klemic, K.G., C.-C. Shieh, G.E. Kirsch, and S.W. Jones. 1998. Biophys. J. 74:1779-1789) in which an absence of the NH(2) terminus results in accelerated inactivation from closed states relative to full-length Kv1 [16].

Regulatory relationships of Kcnb1

  • 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 [17].

Other interactions of Kcnb1

  • Similar to Kv4.3, expression of Kvbeta1, as well as Kv1.5 and Kv2.1, is similar in wild-type and Kv4.2(-/-) ventricles [18].
  • The non-Shaker Kv2.1 channel did not assemble with Kv1.1 or Kv1 [19].
  • In contrast, Kv1.2, Kv1.3, and Kv2.1 showed variable subcellular distribution depending upon cellular context [20].
  • Substitution of linkers from the slowly activating Shab and Shaw channels resulted in a three-to fourfold slowing of activation and deactivation [21].
  • We report here the initial characterization of 18 mutations in the S3-S4 linker of the Shaker channel, including deletions, insertions, charge change, substitution of prolines, and chimeras replacing the 25-residue Shaker linker with 7- or 9-residue sequences from Shab, Shaw, or Shal [21].

Analytical, diagnostic and therapeutic context of Kcnb1


  1. Oxygen sensitivity of cloned voltage-gated K(+) channels expressed in the pulmonary vasculature. Hulme, J.T., Coppock, E.A., Felipe, A., Martens, J.R., Tamkun, M.M. Circ. Res. (1999) [Pubmed]
  2. The K(+) channel gene, Kcnb1: genomic structure and characterization of its 5'-regulatory region as part of an overlapping gene group. Roder, K., Koren, G. Biol. Chem. (2006) [Pubmed]
  3. Inhibition of Kv2.1 voltage-dependent K+ channels in pancreatic beta-cells enhances glucose-dependent insulin secretion. MacDonald, P.E., Sewing, S., Wang, J., Joseph, J.W., Smukler, S.R., Sakellaropoulos, G., Wang, J., Saleh, M.C., Chan, C.B., Tsushima, R.G., Salapatek, A.M., Wheeler, M.B. J. Biol. Chem. (2002) [Pubmed]
  4. Attenuation of I(K,slow1) and I(K,slow2) in Kv1/Kv2DN mice prolongs APD and QT intervals but does not suppress spontaneous or inducible arrhythmias. Kodirov, S.A., Brunner, M., Nerbonne, J.M., Buckett, P., Mitchell, G.F., Koren, G. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  5. 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]
  6. Constitutive activation of delayed-rectifier potassium channels by a src family tyrosine kinase in Schwann cells. Sobko, A., Peretz, A., Attali, B. EMBO J. (1998) [Pubmed]
  7. K+ currents and K+ channel mRNA in cultured atrial cardiac myocytes (AT-1 cells). Yang, T., Wathen, M.S., Felipe, A., Tamkun, M.M., Snyders, D.J., Roden, D.M. Circ. Res. (1994) [Pubmed]
  8. Expression and function of pancreatic beta-cell delayed rectifier K+ channels. Role in stimulus-secretion coupling. Roe, M.W., Worley, J.F., Mittal, A.A., Kuznetsov, A., DasGupta, S., Mertz, R.J., Witherspoon, S.M., Blair, N., Lancaster, M.E., McIntyre, M.S., Shehee, W.R., Dukes, I.D., Philipson, L.H. J. Biol. Chem. (1996) [Pubmed]
  9. Molecular basis of transient outward K+ current diversity in mouse ventricular myocytes. Guo, W., Xu, H., London, B., Nerbonne, J.M. J. Physiol. (Lond.) (1999) [Pubmed]
  10. Regional upregulation of Kv2.1-encoded current, IK,slow2, in Kv1DN mice is abolished by crossbreeding with Kv2DN mice. Zhou, J., Kodirov, S., Murata, M., Buckett, P.D., Nerbonne, J.M., Koren, G. Am. J. Physiol. Heart Circ. Physiol. (2003) [Pubmed]
  11. Modification of Kv2.1 K+ currents by the silent Kv10 subunits. Vega-Saenz de Miera, E.C. Brain Res. Mol. Brain Res. (2004) [Pubmed]
  12. NFATc3 regulates Kv2.1 expression in arterial smooth muscle. Amberg, G.C., Rossow, C.F., Navedo, M.F., Santana, L.F. J. Biol. Chem. (2004) [Pubmed]
  13. Hypomyelination and increased activity of voltage-gated K(+) channels in mice lacking protein tyrosine phosphatase epsilon. Peretz, A., Gil-Henn, H., Sobko, A., Shinder, V., Attali, B., Elson, A. EMBO J. (2000) [Pubmed]
  14. Inhibition of cardiac potassium currents by the vesnarinone analog OPC-18790: comparison with quinidine and dofetilide. Yang, T., Snyders, D.J., Roden, D.M. J. Pharmacol. Exp. Ther. (1997) [Pubmed]
  15. Differential targeting of Shaker-like potassium channels to lipid rafts. Martens, J.R., Navarro-Polanco, R., Coppock, E.A., Nishiyama, A., Parshley, L., Grobaski, T.D., Tamkun, M.M. J. Biol. Chem. (2000) [Pubmed]
  16. Altered state dependence of c-type inactivation in the long and short forms of human Kv1.5. Kurata, H.T., Soon, G.S., Fedida, D. J. Gen. Physiol. (2001) [Pubmed]
  17. 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]
  18. Targeted deletion of Kv4.2 eliminates I(to,f) and results in electrical and molecular remodeling, with no evidence of ventricular hypertrophy or myocardial dysfunction. Guo, W., Jung, W.E., Marionneau, C., Aimond, F., Xu, H., Yamada, K.A., Schwarz, T.L., Demolombe, S., Nerbonne, J.M. Circ. Res. (2005) [Pubmed]
  19. 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]
  20. Identification and localization of K+ channels in the mouse retina. Klumpp, D.J., Song, E.J., Pinto, L.H. Vis. Neurosci. (1995) [Pubmed]
  21. Role of the S3-S4 linker in Shaker potassium channel activation. Mathur, R., Zheng, J., Yan, Y., Sigworth, F.J. J. Gen. Physiol. (1997) [Pubmed]
  22. Hypoxic vasorelaxation inhibition by organ culture correlates with loss of Kv channels but not Ca(2+) channels. Thorne, G.D., Conforti, L., Paul, R.J. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
  23. Striatal potassium channel dysfunction in Huntington's disease transgenic mice. Ariano, M.A., Cepeda, C., Calvert, C.R., Flores-Hernández, J., Hernández-Echeagaray, E., Klapstein, G.J., Chandler, S.H., Aronin, N., DiFiglia, M., Levine, M.S. J. Neurophysiol. (2005) [Pubmed]
  24. Heterologous expression of the human potassium channel Kv2.1 in clonal mammalian cells by direct cytoplasmic microinjection of cRNA. Ikeda, S.R., Soler, F., Zühlke, R.D., Joho, R.H., Lewis, D.L. Pflugers Arch. (1992) [Pubmed]
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