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A Model of the Block of Voltage-Gated Potassium Kv4.2 Ionic Currents by 4-Aminopyridine

The Journal of pharmacology and experimental therapeutics, 2017-11, Vol.363 (2), p.184

Kehl, Steven J

2017

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An Activation Gating Switch in Kv1.2 Is Localized to a Threonine Residue in the S2-S3 Linker

Biophysical journal, 2007-12, Vol.93 (12), p.4173-4186

2007

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Molecular determinants of the inhibition of human Kv1.5 potassium currents by external protons and Zn2

The Journal of physiology, 2002-05, Vol.541 (1), p.9-24

2002

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4-aminopyridine prevents the conformational changes associated with p/c-type inactivation in shaker channels

The Journal of pharmacology and experimental therapeutics, 2007-01, Vol.320 (1), p.162

2007

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External Ba(2+) block of Kv4.2 channels is enhanced in the closed-inactivated state

American Journal of Physiology: Cell Physiology, 2013-02, Vol.304 (4), p.C370-C381

2013

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Modulation of human ether-Ã -go-go-related K+ (HERG) channel inactivation by Cs+ and K

The Journal of physiology, 2003-05, Vol.548 (3), p.691-702

2003

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ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K+o-dependent resting inactivation

Pflügers Archiv, 2013-11, Vol.465 (11), p.1545-1555

2013

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Kinetic analysis of the effects of H+ or Ni2+ on Kv1.5 current shows that both ions enhance slow inactivation and induce resting inactivation

The Journal of physiology, 2010-08, Vol.588 (16), p.3011-3030

2010

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Modulation of Kv1.5 Potassium Channel Gating by Extracellular Zinc

Biophysical journal, 2001-07, Vol.81 (1), p.125-136

2001

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Control of voltage-gated K+ channel permeability to NMDG+ by a residue at the outer pore

The Journal of general physiology, 2009-04, Vol.133 (4), p.361-374

2009

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External K+ relieves the block but not the gating shift caused by Zn2+ in human Kv1.5 potassium channels

The Journal of physiology, 2001-04, Vol.532 (2), p.349-358

2001

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Synergistic inhibition of the maximum conductance of Kv1.5 channels by extracellular K+ reduction and acidification

Cell biochemistry and biophysics, 2005-01, Vol.43 (2), p.231-242

2005

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External Ba2+ block of human Kv1.5 at neutral and acidic pH: evidence for Ho+-induced constriction of the outer pore mouth at rest

Biophysical journal, 2008-11, Vol.95 (9), p.4456-4468

2008

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Molecular determinants of the inhibition of human Kv1.5 potassium currents by external protons and Zn(2+)

The Journal of physiology, 2002-05, Vol.541 (Pt 1), p.9

2002

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A direct demonstration of closed-state inactivation of K+ channels at low pH

The Journal of general physiology, 2007-05, Vol.129 (5), p.437-455

2007

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SCAM analysis reveals a discrete region of the pore turret that modulates slow inactivation in Kv1.5

American Journal of Physiology: Cell Physiology, 2007-03, Vol.292 (3), p.C1041-C1052

2007

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Single Channel Analysis Reveals Different Modes of Kv1.5 Gating Behavior Regulated by Changes of External pH

Biophysical journal, 2006-02, Vol.90 (4), p.1212-1222

2006

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Closed-state inactivation induced in K(V)1 channels by extracellular acidification

Channels (Austin, Tex.), 2008-03, Vol.2 (2), p.139-142

2008

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External Ba 2+ block of Kv4.2 channels is enhanced in the closed-inactivated state

American Journal of Physiology: Cell Physiology, 2013-02, Vol.304 (4), p.C370-C381

2013

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External Ba^sup 2+^ block of Kv4.2 channels is enhanced in the closed-inactivated state

American Journal of Physiology: Cell Physiology, 2013-02, Vol.304 (4), p.C370

2013

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Block by internal Mg2+ causes voltage-dependent inactivation of Kv1.5

European biophysics journal, 2006-12, Vol.36 (1), p.23-34

2006

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External Ba2+ block of Kv4.2 channels is enhanced in the closed-inactivated state

American Journal of Physiology: Cell Physiology, 2013, Vol.73 (2)

2013

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Rapid induction of P/C-type inactivation is the mechanism for acid-induced K+ current inhibition

The Journal of general physiology, 2003-03, Vol.121 (3), p.215-225

2003

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The external K+ concentration and mutations in the outer pore mouth affect the inhibition of kv1.5 current by Ni2

Biophysical journal, 2004-04, Vol.86 (4), p.2238-2250

2004

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ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K^sup +^^sub o^-dependent resting inactivation

Pflügers Archiv, 2013-11, Vol.465 (11), p.1545

2013

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A Model of the Block of Voltage-Gated Potassium Kv4.2 Ionic Currents by 4-Aminopyridine

An Activation Gating Switch in Kv1.2 Is Localized to a Threonine Residue in the S2-S3 Linker

Molecular determinants of the inhibition of human Kv1.5 potassium currents by external protons and Zn2

4-aminopyridine prevents the conformational changes associated with p/c-type inactivation in shaker channels

External Ba(2+) block of Kv4.2 channels is enhanced in the closed-inactivated state

Modulation of human ether-Ã -go-go-related K+ (HERG) channel inactivation by Cs+ and K

ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K+o-dependent resting inactivation

Kinetic analysis of the effects of H+ or Ni2+ on Kv1.5 current shows that both ions enhance slow inactivation and induce resting inactivation

Modulation of Kv1.5 Potassium Channel Gating by Extracellular Zinc

Control of voltage-gated K+ channel permeability to NMDG+ by a residue at the outer pore

External K+ relieves the block but not the gating shift caused by Zn2+ in human Kv1.5 potassium channels

Synergistic inhibition of the maximum conductance of Kv1.5 channels by extracellular K+ reduction and acidification

External Ba2+ block of human Kv1.5 at neutral and acidic pH: evidence for Ho+-induced constriction of the outer pore mouth at rest

Molecular determinants of the inhibition of human Kv1.5 potassium currents by external protons and Zn(2+)

A direct demonstration of closed-state inactivation of K+ channels at low pH

SCAM analysis reveals a discrete region of the pore turret that modulates slow inactivation in Kv1.5

Single Channel Analysis Reveals Different Modes of Kv1.5 Gating Behavior Regulated by Changes of External pH

Closed-state inactivation induced in K(V)1 channels by extracellular acidification

External Ba 2+ block of Kv4.2 channels is enhanced in the closed-inactivated state

External Ba^sup 2+^ block of Kv4.2 channels is enhanced in the closed-inactivated state

Block by internal Mg2+ causes voltage-dependent inactivation of Kv1.5

External Ba2+ block of Kv4.2 channels is enhanced in the closed-inactivated state

Rapid induction of P/C-type inactivation is the mechanism for acid-induced K+ current inhibition

The external K+ concentration and mutations in the outer pore mouth affect the inhibition of kv1.5 current by Ni2

ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K^sup +^^sub o^-dependent resting inactivation

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