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J Physiol
2005 Nov 01;568Pt 3:749-66. doi: 10.1113/jphysiol.2005.085746.
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A difference in inward rectification and polyamine block and permeation between the Kir2.1 and Kir3.1/Kir3.4 K+ channels.
Makary SM
,
Claydon TW
,
Enkvetchakul D
,
Nichols CG
,
Boyett MR
.
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Inward rectification is caused by voltage-dependent block of the channel pore by intracellular Mg2+ and polyamines such as spermine. In the present study, we compared inward rectification in the Kir3.1/Kir3.4 channel, which underlies the cardiac current I(K,ACh), and the Kir2.1 channel, which underlies the cardiac current I(K,1). Sustained outward current at potentials positive to the K+ reversal potential was observed through Kir3.1/Kir3.4, but not Kir2.1, demonstrating that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1. We show that Kir3.1/Kir3.4 is more sensitive to extracellular spermine block than Kir2.1, and that intracellular and extracellular polyamines can permeate Kir3.1/Kir3.4, but not Kir2.1, to a limited extent. We describe a simple kinetic model in which polyamines act as permeant blockers of Kir3.1/Kir3.4, but as relatively impermeant blockers of Kir2.1. The model shows the difference in sensitivity to extracellular spermine block, as well as the difference in the extent of inward rectification between the two channels. This suggests that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1 because of the difference in the balance of polyamine block and permeation of the two channels.
Adrian,
The potassium and chloride conductance of frog muscle membrane.
1962, Pubmed
Adrian,
The potassium and chloride conductance of frog muscle membrane.
1962,
Pubmed
Bähring,
Permeation and block of rat GluR6 glutamate receptor channels by internal and external polyamines.
1997,
Pubmed
Chang,
The effects of spermine on the accessibility of residues in the M2 segment of Kir2.1 channels expressed in Xenopus oocytes.
2003,
Pubmed
,
Xenbase
Dibb,
Molecular basis of ion selectivity, block, and rectification of the inward rectifier Kir3.1/Kir3.4 K(+) channel.
2003,
Pubmed
Dobrzynski,
Effects of ACh and adenosine mediated by Kir3.1 and Kir3.4 on ferret ventricular cells.
2002,
Pubmed
Fakler,
A structural determinant of differential sensitivity of cloned inward rectifier K+ channels to intracellular spermine.
1994,
Pubmed
,
Xenbase
Ficker,
Spermine and spermidine as gating molecules for inward rectifier K+ channels.
1994,
Pubmed
,
Xenbase
Frazier,
Apparent change in ion selectivity caused by changes in intracellular K(+) during whole-cell recording.
2000,
Pubmed
Fujiwara,
Ser165 in the second transmembrane region of the Kir2.1 channel determines its susceptibility to blockade by intracellular Mg2+.
2002,
Pubmed
,
Xenbase
Guo,
Mechanism of IRK1 channel block by intracellular polyamines.
2000,
Pubmed
,
Xenbase
Guo,
Interaction mechanisms between polyamines and IRK1 inward rectifier K+ channels.
2003,
Pubmed
,
Xenbase
Guo,
Mechanism of rectification in inward-rectifier K+ channels.
2003,
Pubmed
,
Xenbase
Hagiwara,
The anomalous rectification and cation selectivity of the membrane of a starfish egg cell.
1974,
Pubmed
Hagiwara,
Anomalous permeabilities of the egg cell membrane of a starfish in K+-Tl+ mixtures.
1977,
Pubmed
Hommers,
Regulation of the inward rectifying properties of G-protein-activated inwardly rectifying K+ (GIRK) channels by Gbeta gamma subunits.
2003,
Pubmed
Ishihara,
Inward rectifier K(+) current under physiological cytoplasmic conditions in guinea-pig cardiac ventricular cells.
2002,
Pubmed
Jin,
A novel high-affinity inhibitor for inward-rectifier K+ channels.
1998,
Pubmed
,
Xenbase
Jin,
Synthesis of a stable form of tertiapin: a high-affinity inhibitor for inward-rectifier K+ channels.
1999,
Pubmed
,
Xenbase
Krapivinsky,
The G-protein-gated atrial K+ channel IKACh is a heteromultimer of two inwardly rectifying K(+)-channel proteins.
1995,
Pubmed
,
Xenbase
Kubo,
Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel.
1993,
Pubmed
,
Xenbase
Kubo,
Control of rectification and permeation by two distinct sites after the second transmembrane region in Kir2.1 K+ channel.
2001,
Pubmed
,
Xenbase
Kurachi,
Voltage-dependent activation of the inward-rectifier potassium channel in the ventricular cell membrane of guinea-pig heart.
1985,
Pubmed
Kurata,
Molecular basis of inward rectification: polyamine interaction sites located by combined channel and ligand mutagenesis.
2004,
Pubmed
,
Xenbase
Lancaster,
Residues and mechanisms for slow activation and Ba2+ block of the cardiac muscarinic K+ channel, Kir3.1/Kir3.4.
2000,
Pubmed
,
Xenbase
Lewis,
Ion-concentration dependence of the reversal potential and the single channel conductance of ion channels at the frog neuromuscular junction.
1979,
Pubmed
Liu,
Comparison of cloned Kir2 channels with native inward rectifier K+ channels from guinea-pig cardiomyocytes.
2001,
Pubmed
,
Xenbase
Lomax,
Electrophysiological evidence for a gradient of G protein-gated K+ current in adult mouse atria.
2003,
Pubmed
Lopatin,
The mechanism of inward rectification of potassium channels: "long-pore plugging" by cytoplasmic polyamines.
1995,
Pubmed
,
Xenbase
Lopatin,
Potassium channel block by cytoplasmic polyamines as the mechanism of intrinsic rectification.
1994,
Pubmed
,
Xenbase
Lu,
Electrostatic tuning of Mg2+ affinity in an inward-rectifier K+ channel.
1994,
Pubmed
,
Xenbase
Ma,
Diverse trafficking patterns due to multiple traffic motifs in G protein-activated inwardly rectifying potassium channels from brain and heart.
2002,
Pubmed
Nichols,
Inward rectification and implications for cardiac excitability.
1996,
Pubmed
Nichols,
Inward rectifier potassium channels.
1997,
Pubmed
Owen,
Effect of extracellular cations on the inward rectifying K+ channels Kir2.1 and Kir3.1/Kir3.4.
1999,
Pubmed
,
Xenbase
Schild,
Competitive binding interaction between Zn2+ and saxitoxin in cardiac Na+ channels. Evidence for a sulfhydryl group in the Zn2+/saxitoxin binding site.
1991,
Pubmed
Shui,
Evidence of involvement of GIRK1/GIRK4 in long-term desensitization of cardiac muscarinic K+ channels.
2001,
Pubmed
Stanfield,
A single aspartate residue is involved in both intrinsic gating and blockage by Mg2+ of the inward rectifier, IRK1.
1994,
Pubmed
Tzounopoulos,
Induction of endogenous channels by high levels of heterologous membrane proteins in Xenopus oocytes.
1995,
Pubmed
,
Xenbase
Woodhull,
Ionic blockage of sodium channels in nerve.
1973,
Pubmed
Xie,
Inward rectification by polyamines in mouse Kir2.1 channels: synergy between blocking components.
2003,
Pubmed
,
Xenbase
Yang,
Regional differences in the negative inotropic effect of acetylcholine within the canine ventricle.
1996,
Pubmed
Yang,
Control of rectification and permeation by residues in two distinct domains in an inward rectifier K+ channel.
1995,
Pubmed
,
Xenbase
Zang,
On the role of G protein activation and phosphorylation in desensitization to acetylcholine in guinea-pig atrial cells.
1993,
Pubmed
Zaritsky,
The consequences of disrupting cardiac inwardly rectifying K(+) current (I(K1)) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes.
2001,
Pubmed
Zeuthen,
Mobility of ions, sugar, and water in the cytoplasm of Xenopus oocytes expressing Na(+)-coupled sugar transporters (SGLT1).
2002,
Pubmed
,
Xenbase
Zobel,
Molecular dissection of the inward rectifier potassium current (IK1) in rabbit cardiomyocytes: evidence for heteromeric co-assembly of Kir2.1 and Kir2.2.
2003,
Pubmed
