Central Charged Residues in DIIIS4 Regulate Deactivation Gating in Skeletal Muscle Sodium Channels

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Cellular and molecular neurobiology

• Publication date

  2007-01-23

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1007/s10571-006-9120-2PMID 17151947PMCID PMC11517295
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Central Charged Residues in DIIIS4 Regulate Deactivation Gating in Skeletal Muscle Sodium Channels

  2007cited by this paper
• Single point mutations of the sodium channel drastically reduce the pore permeability without preventing its gating

  2005cited by this paper
• Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation

  2005cited by this paper
• K-Aggravated Myotonia Mutations at Residue G1306 Differentially Alter Deactivation Gating of Human Skeletal Muscle Sodium Channels

  2005cited by this paper
• Cooperative effect of S4–S5 loops in domains D3 and D4 on fast inactivation of the Na+ channel

  2004influential reference
• Temperature‐sensitive defects in paramyotonia congenita mutants R1448C and T1313M

  2004cited by this paper
• Functional characterization and cold sensitivity of T1313A, a new mutation of the skeletal muscle sodium channel causing paramyotonia congenita in humans

  2004cited by this paper
• Overview of the voltage-gated sodium channel family

  2003cited by this paper
• The Position of the Fourth Segment of Domain 4 Determines Status of the Inactivation Gate in Na+ Channels

  2003cited by this paper
• Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation.

  2002cited by this paper
• The outermost lysine in the S4 of domain III contributes little to the gating charge in sodium channels.

  2002influential reference
• Tracking Voltage-dependent Conformational Changes in Skeletal Muscle Sodium Channel during Activation

  2002influential reference
• Immobilizing the Moving Parts of Voltage-Gated Ion Channels

  2000cited by this paper
• The Delay in Recovery from Fast Inactivation in Skeletal Muscle Sodium Channels Is Deactivation

  2000cited by this paper
• The Role of the Putative Inactivation Lid in Sodium Channel Gating Current Immobilization

  2000influential reference
• From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels.

  2000cited by this paper
• Differential effects of homologous S4 mutations in human skeletal muscle sodium channels on deactivation gating from open and inactivated states

  1999cited by this paper
• The Na channel voltage sensor associated with inactivation is localized to the external charged residues of domain IV, S4.

  1999cited by this paper
• Voltage-gated ion channels and hereditary disease.

  1999cited by this paper
• Movement of Voltage Sensor S4 in Domain 4 Is Tightly Coupled to Sodium Channel Fast Inactivation and Gating Charge Immobilization

  1999influential reference
• Interaction between the Pore and a Fast Gate of the Cardiac Sodium Channel

  1999cited by this paper
• Voltage sensors in domains III and IV, but not I and II, are immobilized by Na+ channel fast inactivation.

  1999cited by this paper
• A defect in skeletal muscle sodium channel deactivation exacerbates hyperexcitability in human paramyotonia congenita

  1998cited by this paper
• A Critical Role for the S4-S5 Intracellular Loop in Domain IV of the Sodium Channel α-Subunit in Fast Inactivation*

  1998cited by this paper
• Independent Versus Coupled Inactivation in Sodium Channels

  1998cited by this paper
• Voltage-Gated Ion Channels Review and Electrical Excitability

  1998influential reference
• Interaction between the sodium channel inactivation linker and domain III S4-S5.

  1997cited by this paper
• Sodium Channel Activation Gating Is Affected by Substitutions of Voltage Sensor Positive Charges in All Four Domains

  1997influential reference
• Sodium Channel Inactivation Is Altered by Substitution of Voltage Sensor Positive Charges

  1997cited by this paper
• The Journal of General Physiology. Volume 110, No. 4,  October 1997.

  1997cited by this paper
• Molecular Analysis of Potential Hinge Residues in the Inactivation Gate of Brain Type IIA Na+ Channels

  1997cited by this paper
• A unique role for the S4 segment of domain 4 in the inactivation of sodium channels

  1996influential reference
• Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker

  1996cited by this paper
• Molecular basis of charge movement in voltage-gated sodium channels.

  1996cited by this paper
• Evidence for voltage-dependent S4 movement in sodium channels.

  1995cited by this paper
• Modification of inactivation in cardiac sodium channels: ionic current studies with Anthopleurin-A toxin

  1995cited by this paper
• Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation.

  1994cited by this paper
• Na+ channels must deactivate to recover from inactivation.

  1994influential reference
• A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.

  1992cited by this paper
• A quantitative description of membrane current and its application to conduction and excitation in nerve. 1952.

  1990cited by this paper
• Structural parts involved in activation and inactivation of the sodium channel

  1989cited by this paper
• Site-directed mutagenesis by overlap extension using the polymerase chain reaction.

  1989cited by this paper
• Identification of an intracellular peptide segment involved in sodium channel inactivation.

  1988cited by this paper
• Primary structure of Electrophorus electricus sodium channel deduced from cDNA sequence

  1984cited by this paper
• Charge Movement Associated with the Opening and Closing of the Activation Gates of the Na Channels

  1974cited by this paper
• A quantitative description of membrane current and its application to conduction and excitation in nerve

  1952cited by this paper

• Hyperkalemic Periodic Paralysis

  2016cites this paper
• Charakterisierung neuer Hypokaliämische Periodische Paralysen verursachender Mutationen in Domäne III des spannungsabhängigen Natriumkanals 1.4 mit Hilfe der Patch-clamp Technik

  2013cites this paper
• Open- and closed-state fast inactivation in sodium channels

  2011cites this paper
• Caractérisation clinique et génétique des myotonies congénitales classiques et atypiques au Saguenay Lac St-Jean

  2010cites this paper
• Charge immobilization of skeletal muscle Na+ channels: role of residues in the inactivation linker.

  2007cites this paper
• Central Charged Residues in DIIIS4 Regulate Deactivation Gating in Skeletal Muscle Sodium Channels

  2007cites this paper
• Role of hydrophobic residues in the voltage sensors of the voltage-gated sodium channel.

  2007cites this paper