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Multiple residues specify external tetraethylammonium blockade in voltage-gated potassium channels.
Pascual JM
,
Shieh CC
,
Kirsch GE
,
Brown AM
.
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We have mapped residues in the carboxyl half of the P region of a voltage-gated K+ channel that influence external tetraethylammonium (TEA) block. Fifteen amino acids were substituted with cysteine and expressed in oocytes from monomeric or heterodimeric cRNAs. From a total of six mutant channels with altered TEA sensitivity, three were susceptible to modification by extracellularly applied charged methanethiosulfonates (MTSX). Another residue did not affect TEA block but was protected from MTSX by TEA. MTSX modification of position Y380C, thought to form the TEA binding site, affected TEA affinity only moderately, and this effect could be reversed by additional charge transfer from an oppositely charged MTSX analog. The results show that TEA block is modulated from multiple sites, including residues located deep in the pore and that several side chains besides that of Y380 are exposed at the TEA receptor.
Akabas,
Acetylcholine receptor channel structure probed in cysteine-substitution mutants.
1992,
Pubmed
,
Xenbase
Akabas,
Identification of acetylcholine receptor channel-lining residues in the entire M2 segment of the alpha subunit.
1994,
Pubmed
,
Xenbase
Armstrong,
Interaction of tetraethylammonium ion derivatives with the potassium channels of giant axons.
1971,
Pubmed
Hartmann,
Exchange of conduction pathways between two related K+ channels.
1991,
Pubmed
,
Xenbase
Heginbotham,
The aromatic binding site for tetraethylammonium ion on potassium channels.
1992,
Pubmed
Heginbotham,
A functional connection between the pores of distantly related ion channels as revealed by mutant K+ channels.
1992,
Pubmed
,
Xenbase
Hille,
The selective inhibition of delayed potassium currents in nerve by tetraethylammonium ion.
1967,
Pubmed
Kavanaugh,
Interaction between tetraethylammonium and amino acid residues in the pore of cloned voltage-dependent potassium channels.
1991,
Pubmed
,
Xenbase
Kavanaugh,
Multiple subunits of a voltage-dependent potassium channel contribute to the binding site for tetraethylammonium.
1992,
Pubmed
,
Xenbase
Kirsch,
Functional role of a conserved aspartate in the external mouth of voltage-gated potassium channels.
1995,
Pubmed
,
Xenbase
Kirsch,
Differences between the deep pores of K+ channels determined by an interacting pair of nonpolar amino acids.
1992,
Pubmed
,
Xenbase
Kürz,
Side-chain accessibilities in the pore of a K+ channel probed by sulfhydryl-specific reagents after cysteine-scanning mutagenesis.
1995,
Pubmed
,
Xenbase
MacKinnon,
Mutations affecting TEA blockade and ion permeation in voltage-activated K+ channels.
1990,
Pubmed
Newland,
Repulsion between tetraethylammonium ions in cloned voltage-gated potassium channels.
1992,
Pubmed
,
Xenbase
Pascual,
K+ pore structure revealed by reporter cysteines at inner and outer surfaces.
1995,
Pubmed
,
Xenbase
Shieh,
Mutational analysis of ion conduction and drug binding sites in the inner mouth of voltage-gated K+ channels.
1994,
Pubmed
Stanfield,
Tetraethylammonium ions and the potassium permeability of excitable cells.
1983,
Pubmed
Yellen,
Mutations affecting internal TEA blockade identify the probable pore-forming region of a K+ channel.
1991,
Pubmed
Yool,
Alteration of ionic selectivity of a K+ channel by mutation of the H5 region.
1991,
Pubmed
,
Xenbase
