Lista de obras - Tom W Claydon - Dominio Público Uruguay

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

artículo científico publicado en 2006

A difference in inward rectification and polyamine block and permeation between the Kir2.1 and Kir3.1/Kir3.4 K+ channels

artículo científico publicado en 2005

An activation gating switch in Kv1.2 is localized to a threonine residue in the S2-S3 linker.

artículo científico publicado en 2007

Base of pore loop is important for rectification, activation, permeation, and block of Kir3.1/Kir3.4.

artículo científico publicado en 2006

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

scientific article published on 11 August 2006

Correction

External protons destabilize the activated voltage sensor in hERG channels.

artículo científico publicado en 2013

Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.

artículo científico publicado en 2011

Extracellular protons accelerate hERG channel deactivation by destabilizing voltage sensor relaxation

scientific article published on 07 December 2018

Functional interactions of voltage sensor charges with an S2 hydrophobic plug in hERG channels

artículo científico publicado en 2013

Inhibition of the K+ channel kv1.4 by acidosis: protonation of an extracellular histidine slows the recovery from N-type inactivation

artículo científico publicado en 2000

Ion channel model reduction using manifold boundaries

artículo científico publicado en 2022

KN-93 (2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine), a calcium/calmodulin-dependent protein kinase II inhibitor, is a direct extracellular blocker of voltage-gated potassium channels.

artículo científico publicado en 2005

Loss-of-Function and Gain-of-Function Mutations in KCNQ5 Cause Intellectual Disability or Epileptic Encephalopathy

artículo científico publicado en 2017

Molecular basis of ion selectivity, block, and rectification of the inward rectifier Kir3.1/Kir3.4 K(+) channel

artículo científico publicado en 2003

Molecular determinants of U-type inactivation in Kv2.1 channels

artículo científico publicado en 2011

Mutations within the S4-S5 linker alter voltage sensor constraints in hERG K+ channels

artículo científico publicado en 2010

NS1643 interacts around L529 of hERG to alter voltage sensor movement on the path to activation.

artículo científico publicado en 2015

Photothermal release of small molecules from gold nanoparticles in live cells ⬇️

artículo científico publicado el 16 de noviembre de 2011

Polyunsaturated fatty acids inhibit Kv1.4 by interacting with positively charged extracellular pore residues

artículo científico publicado en 2016

Proline scan of the HERG channel S6 helix reveals the location of the intracellular pore gate.

artículo científico publicado en 2014

Proton block of the pore underlies the inhibition of hERG cardiac K+ channels during acidosis

artículo científico publicado en 2012

Proton sensors in the pore domain of the cardiac voltage-gated sodium channel

artículo científico publicado en 2013

Rapid outer pore movements after opening in a KV1 potassium channel are revealed by TMRM fluorescence from the S3-S4 linker, and modulated by extracellular potassium

artículo científico publicado en 2009

Regional flexibility in the S4-S5 linker regulates hERG channel closed-state stabilization

artículo científico publicado en 2014

Role of internalization of M2 muscarinic receptor via clathrin-coated vesicles in desensitization of the muscarinic K+ current in heart

scientific article published on 29 September 2006

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

artículo científico publicado en 2006

Stabilization of the Activated hERG Channel Voltage Sensor by Depolarization Involves the S4-S5 Linker

artículo científico publicado en 2017

The Selectivity Filter May Act as the Agonist-activated Gate in the G Protein-activated Kir3.1/Kir3.4 K+ Channel ⬇️

artículo científico publicado el 2 de octubre de 2003

The Zebrafish Heart as a Model of Mammalian Cardiac Function

artículo científico publicado en 2016

Two pore residues mediate acidosis-induced enhancement of C-type inactivation of the Kv1.4 K(+) channel

artículo científico publicado en 2002

Voltage clamp fluorimetry reveals a novel outer pore instability in a mammalian voltage-gated potassium channel.

artículo científico publicado en 2008

Voltage clamp fluorimetry studies of mammalian voltage-gated K(+) channel gating.

artículo científico publicado en 2007

Lista de obras de Tom W Claydon

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

A difference in inward rectification and polyamine block and permeation between the Kir2.1 and Kir3.1/Kir3.4 K+ channels

An activation gating switch in Kv1.2 is localized to a threonine residue in the S2-S3 linker.

Base of pore loop is important for rectification, activation, permeation, and block of Kir3.1/Kir3.4.

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

Correction

External protons destabilize the activated voltage sensor in hERG channels.

Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.

Extracellular protons accelerate hERG channel deactivation by destabilizing voltage sensor relaxation

Functional interactions of voltage sensor charges with an S2 hydrophobic plug in hERG channels

Inhibition of the K+ channel kv1.4 by acidosis: protonation of an extracellular histidine slows the recovery from N-type inactivation

Ion channel model reduction using manifold boundaries

KN-93 (2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine), a calcium/calmodulin-dependent protein kinase II inhibitor, is a direct extracellular blocker of voltage-gated potassium channels.

Loss-of-Function and Gain-of-Function Mutations in KCNQ5 Cause Intellectual Disability or Epileptic Encephalopathy

Molecular basis of ion selectivity, block, and rectification of the inward rectifier Kir3.1/Kir3.4 K(+) channel

Molecular determinants of U-type inactivation in Kv2.1 channels

Mutations within the S4-S5 linker alter voltage sensor constraints in hERG K+ channels

NS1643 interacts around L529 of hERG to alter voltage sensor movement on the path to activation.

Photothermal release of small molecules from gold nanoparticles in live cells ⬇️

Polyunsaturated fatty acids inhibit Kv1.4 by interacting with positively charged extracellular pore residues

Proline scan of the HERG channel S6 helix reveals the location of the intracellular pore gate.

Proton block of the pore underlies the inhibition of hERG cardiac K+ channels during acidosis

Proton sensors in the pore domain of the cardiac voltage-gated sodium channel

Rapid outer pore movements after opening in a KV1 potassium channel are revealed by TMRM fluorescence from the S3-S4 linker, and modulated by extracellular potassium

Regional flexibility in the S4-S5 linker regulates hERG channel closed-state stabilization

Role of internalization of M2 muscarinic receptor via clathrin-coated vesicles in desensitization of the muscarinic K+ current in heart

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

Stabilization of the Activated hERG Channel Voltage Sensor by Depolarization Involves the S4-S5 Linker

The Selectivity Filter May Act as the Agonist-activated Gate in the G Protein-activated Kir3.1/Kir3.4 K+ Channel ⬇️

The Zebrafish Heart as a Model of Mammalian Cardiac Function

Two pore residues mediate acidosis-induced enhancement of C-type inactivation of the Kv1.4 K(+) channel

Voltage clamp fluorimetry reveals a novel outer pore instability in a mammalian voltage-gated potassium channel.

Voltage clamp fluorimetry studies of mammalian voltage-gated K(+) channel gating.