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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 (MaxiK[alpha]) encoded by a single gene, Slo, holding multiple alternative exons. Depending on the tissue, MaxiK[alpha] can associate with modulatory [beta]-subunits ([beta]1-[beta]4) 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[alpha]-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[alpha] 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[alpha] 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.

Copyright (C) 2006 Blackwell Publishing Ltd.