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Symposium Reports |
1 Department of Anaesthesiology, Division of Molecular Medicine
2 Department of Molecular and Medical Pharmacology
3 Department of Physiology
4 Cardiovascular Research Laboratory, University of California Los Angeles, Los Angeles, CA 90095-7115, USA
The basic functional unit of the large-conductance, voltage- and Ca2+-activated K+ (MaxiK, BK, BKCa) channel is a tetramer of the pore-forming 
-subunit (MaxiK) encoded by a single gene, Slo, holding multiple alternative exons. Depending on the tissue, MaxiK can associate with modulatory ß-subunits (ß1–ß4) 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 MaxiK-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 MaxiK 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 MaxiK 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.
(Received 16 September 2005;
accepted after revision 20 October 2005;
first published online 20 October 2005)
Corresponding author L. Toro: Dept. Anesthesiology, UCLA, BH-509A CHS, Box 957115, Los Angeles, CA 90095-7115, USA. Email: ltoro{at}ucla.edu
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