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.
Cysteines in the Shaker K+ channel are not essential for channel activity or zinc modulation.
Boland LM
,
Jurman ME
,
Yellen G
.
???displayArticle.abstract???
We investigated whether the cysteine residues in Shaker potassium (K+) channels are essential for activation and inactivation gating or for modulation of activation gating by external zinc (Zn2+). Mutants of the Shaker K+ channel were prepared in which all seven cysteine residues were replaced (C-less). These changes were made in both wild-type Shaker H4 channels and in a deletion mutant (delta 6-46) lacking N-type ("fast") inactivation. Replacement of all cysteines left most functional properties of the K+ currents unaltered. The most noticeable difference between the C-less and wild-type currents was the faster C-type inactivation of the C-less channel which could be attributed largely to the mutation of Cys462. This is consistent with the effects of previously reported mutations of nearby residues in the S6 region. There were also small changes in the activation gating of C-less currents. Modulation by external Zn2+ of the voltage dependence and rate of activation gating is preserved in the C-less channels, indicating that none of the cysteines in the Shaker K+ channel plays an important role in Zn2+ modulation.
Choi,
Tetraethylammonium blockade distinguishes two inactivation mechanisms in voltage-activated K+ channels.
1991, Pubmed
Choi,
Tetraethylammonium blockade distinguishes two inactivation mechanisms in voltage-activated K+ channels.
1991,
Pubmed
Freedman,
The function and structure of the metal coordination sites within the glucocorticoid receptor DNA binding domain.
1988,
Pubmed
,
Xenbase
Gilly,
Divalent cations and the activation kinetics of potassium channels in squid giant axons.
1982,
Pubmed
Hanas,
Xenopus transcription factor A requires zinc for binding to the 5 S RNA gene.
1983,
Pubmed
,
Xenbase
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
Kamb,
Multiple products of the Drosophila Shaker gene may contribute to potassium channel diversity.
1988,
Pubmed
Kao,
Acetylcholine receptor binding site contains a disulfide cross-link between adjacent half-cystinyl residues.
1986,
Pubmed
Kobayashi,
Nitrilase in biosynthesis of the plant hormone indole-3-acetic acid from indole-3-acetonitrile: cloning of the Alcaligenes gene and site-directed mutagenesis of cysteine residues.
1993,
Pubmed
Kunkel,
Rapid and efficient site-specific mutagenesis without phenotypic selection.
1985,
Pubmed
Lopez,
Hydrophobic substitution mutations in the S4 sequence alter voltage-dependent gating in Shaker K+ channels.
1991,
Pubmed
,
Xenbase
López-Barneo,
Effects of external cations and mutations in the pore region on C-type inactivation of Shaker potassium channels.
1993,
Pubmed
,
Xenbase
MacKinnon,
Determination of the subunit stoichiometry of a voltage-activated potassium channel.
1991,
Pubmed
,
Xenbase
McCormack,
A role for hydrophobic residues in the voltage-dependent gating of Shaker K+ channels.
1991,
Pubmed
,
Xenbase
Mishina,
Location of functional regions of acetylcholine receptor alpha-subunit by site-directed mutagenesis.
,
Pubmed
,
Xenbase
Pan,
Structure and function of the Zn(II) binding site within the DNA-binding domain of the GAL4 transcription factor.
1989,
Pubmed
Ruppersberg,
Regulation of fast inactivation of cloned mammalian IK(A) channels by cysteine oxidation.
1991,
Pubmed
,
Xenbase
Sanger,
DNA sequencing with chain-terminating inhibitors.
1977,
Pubmed
Spires,
Chemical properties of the divalent cation binding site on potassium channels.
1992,
Pubmed
Vallee,
Zinc coordination, function, and structure of zinc enzymes and other proteins.
1990,
Pubmed
Yellen,
Mutations affecting internal TEA blockade identify the probable pore-forming region of a K+ channel.
1991,
Pubmed
Zavitz,
Helicase-deficient cysteine to glycine substitution mutants of Escherichia coli replication protein PriA retain single-stranded DNA-dependent ATPase activity. Zn2+ stimulation of mutant PriA helicase and primosome assembly activities.
1993,
Pubmed