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Biophys J
2003 Jun 01;846:3717-29. doi: 10.1016/S0006-3495(03)75100-5.
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Contribution of cytosolic cysteine residues to the gating properties of the Kir2.1 inward rectifier.
Garneau L
,
Klein H
,
Parent L
,
Sauvé R
.
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The topological model proposed for the Kir2.1 inward rectifier predicts that seven of the channel 13 cysteine residues are distributed along the N- and C-terminus regions, with some of the residues comprised within highly conserved domains involved in channel gating. To determine if cytosolic cysteine residues contribute to the gating properties of Kir2.1, each of the N- and C-terminus cysteines was mutated into either a polar (S, D, N), an aliphatic (A,V, L), or an aromatic (W) residue. Our patch-clamp measurements show that with the exception of C76 and C311, the mutation of individual cytosolic cysteine to serine (S) did not significantly affect the single-channel conductance nor the channel open probability. However, mutating C76 to a charged or polar residue resulted either in an absence of channel activity or a decrease in open probability. In turn, the mutations C311S (polar), C311R (charged), and to a lesser degree C311A (aliphatic) led to an increase of the channel mean closed time due to the appearance of long closed time intervals (T(c) >or= 500 ms) and to a reduction of the reactivation by ATP of rundown Kir2.1 channels. These changes could be correlated with a weakening of the interaction between Kir2.1 and PIP(2), with C311R and C311S being more potent at modulating the Kir2.1-PIP(2) interaction than C311A. The present work supports, therefore, molecular models whereby the gating properties of Kir2.1 depend on the presence of nonpolar or neutral residues at positions 76 and 311, with C311 modulating the interaction between Kir2.1 and PIP(2).
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Bannister,
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,
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Cho,
Two critical cysteine residues implicated in disulfide bond formation and proper folding of Kir2.1.
2000,
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,
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Choe,
Structural determinants of gating in inward-rectifier K+ channels.
1999,
Pubmed
,
Xenbase
Choe,
A conserved cytoplasmic region of ROMK modulates pH sensitivity, conductance, and gating.
1997,
Pubmed
,
Xenbase
Cukras,
Structural and functional determinants of conserved lipid interaction domains of inward rectifying Kir6.2 channels.
2002,
Pubmed
Denicourt,
Evidence from incorporation experiments for an anionic channel of small conductance at the apical membrane of the rabbit distal tubule.
1996,
Pubmed
Derst,
Mutations in the ROMK gene in antenatal Bartter syndrome are associated with impaired K+ channel function.
1997,
Pubmed
Elam,
The role of Mg2+ in the inactivation of inwardly rectifying K+ channels in aortic endothelial cells.
1995,
Pubmed
Enkvetchakul,
The kinetic and physical basis of K(ATP) channel gating: toward a unified molecular understanding.
2000,
Pubmed
Fakler,
Strong voltage-dependent inward rectification of inward rectifier K+ channels is caused by intracellular spermine.
1995,
Pubmed
,
Xenbase
Jones,
Multiple sites of interaction between the intracellular domains of an inwardly rectifying potassium channel, Kir6.2.
2001,
Pubmed
Karplus,
Hidden Markov models for detecting remote protein homologies.
1998,
Pubmed
Klein,
Molecular characterization of an inwardly rectifying K+ channel from HeLa cells.
1999,
Pubmed
,
Xenbase
Leyland,
The possible role of a disulphide bond in forming functional Kir2.1 potassium channels.
1999,
Pubmed
Liou,
Regulation of ROMK1 channel by protein kinase A via a phosphatidylinositol 4,5-bisphosphate-dependent mechanism.
1999,
Pubmed
,
Xenbase
Lopes,
Alterations in conserved Kir channel-PIP2 interactions underlie channelopathies.
2002,
Pubmed
,
Xenbase
Lu,
Cytoplasmic amino and carboxyl domains form a wide intracellular vestibule in an inwardly rectifying potassium channel.
1999,
Pubmed
,
Xenbase
Lu,
Electrostatic tuning of Mg2+ affinity in an inward-rectifier K+ channel.
1994,
Pubmed
,
Xenbase
Lu,
Architecture of a K+ channel inner pore revealed by stoichiometric covalent modification.
1999,
Pubmed
,
Xenbase
Morier,
Analysis of a novel double-barreled anion channel from rat liver rough endoplasmic reticulum.
1994,
Pubmed
Nishida,
Structural basis of inward rectification: cytoplasmic pore of the G protein-gated inward rectifier GIRK1 at 1.8 A resolution.
2002,
Pubmed
Plaster,
Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome.
2001,
Pubmed
,
Xenbase
Qin,
Estimating single-channel kinetic parameters from idealized patch-clamp data containing missed events.
1996,
Pubmed
,
Xenbase
Qin,
Maximum likelihood estimation of aggregated Markov processes.
1997,
Pubmed
Roux,
A general solution to the time interval omission problem applied to single channel analysis.
1985,
Pubmed
Ruppersberg,
Intracellular regulation of inward rectifier K+ channels.
2000,
Pubmed
Ruppersberg,
Complexity of the regulation of Kir2.1 K+ channels.
1996,
Pubmed
,
Xenbase
Schulte,
pH gating of ROMK (K(ir)1.1) channels: control by an Arg-Lys-Arg triad disrupted in antenatal Bartter syndrome.
1999,
Pubmed
Shyng,
Structural determinants of PIP(2) regulation of inward rectifier K(ATP) channels.
2000,
Pubmed
Silver,
Intrinsic gating of inward rectifier in bovine pulmonary artery endothelial cells in the presence or absence of internal Mg2+.
1990,
Pubmed
Wible,
Gating of inwardly rectifying K+ channels localized to a single negatively charged residue.
1994,
Pubmed
,
Xenbase
