Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Interactions of the H5 pore region and hydroxylamine with N-type inactivation in the Shaker K+ channel.
Yool AJ
,
Schwarz TL
.
???displayArticle.abstract???
Mutations at sites in the H5 region of the Shaker B K+ channel were used to analyze the influence of the pore on N-type inactivation. Single-channel and two-electrode voltage clamp analyses showed that mutations at residues T441 and T442, which are thought to lie at the internal mouth of the pore, produced opposite effects on inactivation: the inactivated state is stabilized by T441S and destabilized by T442S. In addition, an ammonium derivative, hydroxylamine (OH-(NH3)+), appears to bind in the pore region of T441S and further decreases the rate of recovery from N-type inactivation. This effect relies on the presence of the amino-terminal. The effect of hydroxylamine on the T441S mutation of this K+ channel shows several properties analogous to those of local anesthetics on the Na+ channel. These results can be interpreted to suggest that part of the H5 region contributes to the receptor for the inactivation particle and that a hydroxylamine ion trapped near that site can stabilize their interaction.
Armstrong,
Inactivation of the sodium channel. II. Gating current experiments.
1977, Pubmed
Armstrong,
Inactivation of the sodium channel. II. Gating current experiments.
1977,
Pubmed
Armstrong,
Interaction of tetraethylammonium ion derivatives with the potassium channels of giant axons.
1971,
Pubmed
Barish,
A transient calcium-dependent chloride current in the immature Xenopus oocyte.
1983,
Pubmed
,
Xenbase
Chernoff,
Kinetics of local anesthetic inhibition of neuronal sodium currents. pH and hydrophobicity dependence.
1990,
Pubmed
Choi,
Tetraethylammonium blockade distinguishes two inactivation mechanisms in voltage-activated K+ channels.
1991,
Pubmed
Courtney,
Mechanism of frequency-dependent inhibition of sodium currents in frog myelinated nerve by the lidocaine derivative GEA.
1975,
Pubmed
Demo,
The inactivation gate of the Shaker K+ channel behaves like an open-channel blocker.
1991,
Pubmed
Foster,
A peptide derived from the Shaker B K+ channel produces short and long blocks of reconstituted Ca(2+)-dependent K+ channels.
1992,
Pubmed
Hartmann,
Exchange of conduction pathways between two related K+ channels.
1991,
Pubmed
,
Xenbase
Heginbotham,
A functional connection between the pores of distantly related ion channels as revealed by mutant K+ channels.
1992,
Pubmed
,
Xenbase
Hille,
Common mode of action of three agents that decrease the transient change in sodium permeability in nerves.
1966,
Pubmed
Hille,
Local anesthetics: hydrophilic and hydrophobic pathways for the drug-receptor reaction.
1977,
Pubmed
Hoshi,
Biophysical and molecular mechanisms of Shaker potassium channel inactivation.
1990,
Pubmed
,
Xenbase
Hoshi,
Two types of inactivation in Shaker K+ channels: effects of alterations in the carboxy-terminal region.
1991,
Pubmed
,
Xenbase
Isacoff,
Putative receptor for the cytoplasmic inactivation gate in the Shaker K+ channel.
1991,
Pubmed
,
Xenbase
Iverson,
A-type potassium channels expressed from Shaker locus cDNA.
1988,
Pubmed
,
Xenbase
Jan,
A superfamily of ion channels.
1990,
Pubmed
MacKinnon,
Mutations affecting TEA blockade and ion permeation in voltage-activated K+ channels.
1990,
Pubmed
MacKinnon,
Mutant potassium channels with altered binding of charybdotoxin, a pore-blocking peptide inhibitor.
1989,
Pubmed
,
Xenbase
Motulsky,
Fitting curves to data using nonlinear regression: a practical and nonmathematical review.
1987,
Pubmed
Schwarz,
Multiple potassium-channel components are produced by alternative splicing at the Shaker locus in Drosophila.
1988,
Pubmed
Solaro,
Trypsin-sensitive, rapid inactivation of a calcium-activated potassium channel.
1992,
Pubmed
Tempel,
Sequence of a probable potassium channel component encoded at Shaker locus of Drosophila.
1987,
Pubmed
Timpe,
Four cDNA clones from the Shaker locus of Drosophila induce kinetically distinct A-type potassium currents in Xenopus oocytes.
1988,
Pubmed
,
Xenbase
Toro,
Internal blockade of a Ca(2+)-activated K+ channel by Shaker B inactivating "ball" peptide.
1992,
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
Zagotta,
Restoration of inactivation in mutants of Shaker potassium channels by a peptide derived from ShB.
1990,
Pubmed
,
Xenbase
Zagotta,
Voltage-dependent gating of Shaker A-type potassium channels in Drosophila muscle.
1990,
Pubmed
Zagotta,
Gating of single Shaker potassium channels in Drosophila muscle and in Xenopus oocytes injected with Shaker mRNA.
1989,
Pubmed
,
Xenbase
