Functional consequences of a Na+ channel mutation causing hyperkalemic periodic paralysis.

No abstract is available for this paper.

• Publication year

  1993

• Venue

  Neuron

• Publication date

  1993-04-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/0896-6273(93)90168-QPMID 8386527
• 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.

• Functional expression of sodium channel mutations identified in families with periodic paralysis.

  1993cited by this paper
• muI Na+ channels expressed transiently in human embryonic kidney cells: biochemical and biophysical properties.

  1992cited by this paper
• Putative receptor for the cytoplasmic inactivation gate in the Shaker K+ channel

  1991cited by this paper
• A Met-to-Val mutation in the skeletal muscle Na+ channel α-subunit in hyperkalaemic periodic paralysis

  1991cited by this paper
• Altered gating and conductance of Na+ channels in hyperkalemic periodic paralysis

  1991cited by this paper
• A role for hydrophobic residues in the voltage-dependent gating of Shaker K+ channels.

  1991cited by this paper
• Identification of a mutation in the gene causing hyperkalemic periodic paralysis.

  1991cited by this paper
• A sodium channel defect in hyperkalemic periodic paralysis: potassium-induced failure of inactivation.

  1991cited by this paper
• Analysis in a large hyperkalemic periodic paralysis pedigree supports tight linkage to a sodium channel locus.

  1991cited by this paper
• Multiple gating modes and the effect of modulating factors on the μI sodium channel

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  1990cited by this paper
• Alterations in activation gating of single Shaker A-type potassium channels by the Sh5 mutation

  1990cited by this paper
• Fast and slow gating of sodium channels encoded by a single mRNA.

  1990cited by this paper
• Modulation of ATP-sensitive K+ channels in skeletal muscle by intracellular protons

  1990cited by this paper
• Hyperkalemic periodic paralysis and the adult muscle sodium channel alpha-subunit gene.

  1990cited by this paper
• Primary structure and functional expression of a mammalian skeletal muscle sodium channel.

  1989cited by this paper
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  1989cited by this paper
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  1988cited by this paper
• A rat brain Na+ channel alpha subunit with novel gating properties.

  1988cited by this paper
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  1988cited by this paper
• AAEE minimonograph #27: Differential diagnosis of myotonic syndromes

  1987cited by this paper
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  1987cited by this paper
• Exercise and rest in hyperkalemic periodic paralysis

  1986cited by this paper
• Membrane changes in cells from myotonia patients.

  1985cited by this paper
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  1985cited by this paper
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  1983cited by this paper
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  1980cited by this paper
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  1977cited by this paper
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• Post-exercise increment in compound muscle action potential amplitude in hyperkalemic periodic paralysis.

  2014cites this paper
• Contractile abnormalities of mouse muscles expressing hyperkalemic periodic paralysis mutant NaV1.4 channels do not correlate with Na+ influx or channel content.

  2014cites this paper
• Reduction In Skeletal Muscle Chloride Conductance Improves Contractile Force In Wildtype, But Not In Hyperkalemic Periodic Paralysis Mice

  2014cites this paper
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  2013cites this paper
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