MaxiK channel partners: physiological impact

J Physiol. 2006 Jan 1;570(Pt 1):65-72. doi: 10.1113/jphysiol.2005.098913. Epub 2005 Oct 20.


The basic functional unit of the large-conductance, voltage- and Ca2+-activated K+ (MaxiK, BK, BKCa) channel is a tetramer of the pore-forming alpha-subunit (MaxiKalpha) encoded by a single gene, Slo, holding multiple alternative exons. Depending on the tissue, MaxiKalpha can associate with modulatory beta-subunits (beta1-beta4) increasing its functional diversity. As MaxiK senses and regulates membrane voltage and intracellular Ca2+, it links cell excitability with cell signalling and metabolism. Thus, MaxiK is a key regulator of vital body functions, like blood flow, uresis, immunity and neurotransmission. Epilepsy with paroxysmal dyskinesia syndrome has been recognized as a MaxiKalpha-related disorder caused by a gain-of-function C-terminus mutation. This channel region is also emerging as a key recognition module containing sequences for MaxiKalpha interaction with its surrounding signalling partners, and its targeting to cell-specific microdomains. The growing list of interacting proteins highlights the possibility that associations with the C-terminus of MaxiKalpha are dynamic and depending on each cellular environment. We speculate that the molecular multiplicity of the C-terminus (and intracellular loops) dictated by alternative exons may modulate or create additional interacting sites in a tissue-specific manner. A challenge is the dissection of MaxiK macromolecular signalling complexes in different tissues and their temporal association/dissociation according to the stimulus.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium Signaling / physiology
  • Caveolin 1 / metabolism
  • Epilepsy / genetics
  • Epilepsy / metabolism
  • Humans
  • Hypertension / metabolism
  • Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / genetics
  • Large-Conductance Calcium-Activated Potassium Channel beta Subunits / metabolism*
  • Large-Conductance Calcium-Activated Potassium Channels / metabolism*
  • Membrane Potentials / physiology
  • Muscle, Smooth / metabolism
  • Mutation
  • Protein Kinases / metabolism
  • Receptors, Adrenergic, beta-2 / metabolism


  • Caveolin 1
  • Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
  • Large-Conductance Calcium-Activated Potassium Channel beta Subunits
  • Large-Conductance Calcium-Activated Potassium Channels
  • Receptors, Adrenergic, beta-2
  • Protein Kinases