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Gene Review

Kcnmb1  -  potassium large conductance calcium...

Mus musculus

Synonyms: BK channel beta subunit, BK channel subunit beta-1, BKbeta, BKbeta1, Calcium-activated potassium channel subunit beta, ...
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High impact information on Kcnmb1

  • Using immunohistochemical techniques, we found that BK-beta1 was strongly expressed in the apical membrane of the murine distal nephron and that 98% of BK-beta1 protein detected by histochemistry colocalized with NCX, a marker of connecting tubules (CNT) [1].
  • Potassium chloride- and iberiotoxin-induced depolarization mimicked the effect of BKbeta1-deletion by increasing vascular O2- in an NADPH-dependent fashion [2].
  • NADPH oxidase accounts for enhanced superoxide production and impaired endothelium-dependent smooth muscle relaxation in BKbeta1-/- mice [2].
  • We propose that the elevated blood pressure in BKbeta1 -/- mice serves to normalize Ca(2+) spark/STOC coupling for regulating myogenic tone [3].
  • BK channels are composed of channel-forming BKalpha and auxiliary BKbeta1 subunits, which confer to BK channels an increased sensitivity for changes in membrane potential and Ca(2+) [3].

Biological context of Kcnmb1


Anatomical context of Kcnmb1


Associations of Kcnmb1 with chemical compounds

  • These data show that the BK-beta1 accessory subunit is present in the CNT segment of the mammalian distal nephron and has a significant role in the kaliuretic response to increased urinary flow induced by volume expansion [1].
  • Because the BK-beta1 subunit enhances Ca(2+) sensitivity of BK in a variety of cells, we determined its role in flow-induced K(+) secretion and its localization in the mammalian nephron [1].
  • CONCLUSIONS: The deletion of BKbeta1 causes endothelial dysfunction by increasing O2- formation via increasing activity and expression of the vascular NADPH oxidase [2].


  1. BK-{beta}1 subunit: immunolocalization in the mammalian connecting tubule and its role in the kaliuretic response to volume expansion. Pluznick, J.L., Wei, P., Grimm, P.R., Sansom, S.C. Am. J. Physiol. Renal Physiol. (2005) [Pubmed]
  2. NADPH oxidase accounts for enhanced superoxide production and impaired endothelium-dependent smooth muscle relaxation in BKbeta1-/- mice. Oelze, M., Warnholtz, A., Faulhaber, J., Wenzel, P., Kleschyov, A.L., Coldewey, M., Hink, U., Pongs, O., Fleming, I., Wassmann, S., Meinertz, T., Ehmke, H., Daiber, A., Münzel, T. Arterioscler. Thromb. Vasc. Biol. (2006) [Pubmed]
  3. Mice with disrupted BK channel beta1 subunit gene feature abnormal Ca(2+) spark/STOC coupling and elevated blood pressure. Plüger, S., Faulhaber, J., Fürstenau, M., Löhn, M., Waldschütz, R., Gollasch, M., Haller, H., Luft, F.C., Ehmke, H., Pongs, O. Circ. Res. (2000) [Pubmed]
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