Elsevier

Genomics

Volume 57, Issue 2, 15 April 1999, Pages 323-331
Genomics

Minireview
Evolution and Diversity of Mammalian Sodium Channel Genes

https://doi.org/10.1006/geno.1998.5735Get rights and content

First page preview

First page preview
Click to open first page preview

References (89)

  • L.L. Isom et al.

    Auxiliary subunits of voltage-gated ion channels

    Neuron

    (1994)
  • L.L. Isom et al.

    Structure and function of the β2 subunit of brain sodium channels, a transmembrane glycoprotein with a CAM motif

    Cell

    (1995)
  • J.M. Jones et al.

    Scn2b,

    Genomics

    (1996)
  • K. Loughney et al.

    Molecular analysis of theparaDrosophila

    Cell

    (1989)
  • L.G. Lundin

    Evolution of the vertebrate genome as reflected in paralogous chromosomal regions in man and the house mouse

    Genomics

    (1993)
  • N. Makita et al.

    Genomic organization and chromosomal assignment of the human voltage-gated Na(+) channel β-1 subunit gene (SCN1B

    Genomics

    (1994)
  • K.A. McCormick et al.

    Molecular determinants of Na+

    J. Biol. Chem.

    (1998)
  • D.J. Messner et al.

    The sodium channel from rat brain: Separation and characterization of subunits

    J. Biol. Chem.

    (1985)
  • B.J. Murphy et al.

    cAMP-dependent phosphorylation of two sites in the alpha subunit of the cardiac sodium channel

    J. Biol. Chem.

    (1996)
  • Y. Okamura et al.

    Neural expression of a sodium channel gene requires cell-specific interactions

    Neuron

    (1994)
  • D.E. Patton et al.

    The adult brain β1 subunit modifies activation and inactivation gating of multiple sodium channel α subunits

    J. Biol. Chem.

    (1994)
  • N.W. Plummer et al.

    Exon organization, coding sequence, physical mapping, and polymorphic intragenic markers for the human neuronal sodium channel geneSCN8A

    Genomics

    (1998)
  • N.W. Plummer et al.

    Alternative splicing of the sodium channel SCN8A predicts a truncated two-domain protein in fetal brain and non-neuronal cells

    J. Biol. Chem.

    (1997)
  • J.F. Potts et al.

    A glial-specific voltage-sensitive Na channel gene maps close to clustered genes for neuronal isoforms on mouse chromosome 2

    Biochem. Biophys. Res. Commun.

    (1993)
  • L.J. Ptacek et al.

    Identification of a mutation in the gene causing hyperkalemic periodic paralysis

    Cell

    (1991)
  • Y. Qu et al.

    Modulation of cardiac Na+Xenopus

    J. Biol. Chem.

    (1995)
  • D.S. Ragsdale et al.

    Sodium channels as molecular targets for antiepileptic drugs

    Brain Res. Brain Res. Rev.

    (1998)
  • I.M. Raman et al.

    Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons ofScn8a

    Neuron

    (1997)
  • L. Sangameswaran et al.

    Structure and function of a novel voltage-gated, tetrodotoxin resistant sodium channel specific for sensory neurons

    J. Biol. Chem.

    (1996)
  • C. Sato et al.

    Primary structure of squid sodium channel deduced from the complementary DNA sequence

    Biochem. Biophys. Res. Commun.

    (1992)
  • V.A. Souslova et al.

    Cloning and characterization of a mouse sensory neuron tetrodotoxin-resistant voltage-gated sodium channel geneScn10a

    Genomics

    (1997)
  • C.P. Taylor et al.

    Sodium channels and therapy of central nervous system diseases

    Adv. Pharmacol.

    (1997)
  • Q. Wang et al.

    SCN5A mutations associated with an inherited cardiac arrhythmia, Long QT syndrome

    Cell

    (1995)
  • Q. Wang et al.

    Genomic organization of the humanSCN5A

    Genomics

    (1996)
  • D.A. Wollner et al.

    β2 subunits of sodium channels from vertebrate brain: Studies with subunit-specific antibodies

    J. Biol. Chem.

    (1987)
  • J.S. Yang et al.

    Expression of the sodium channel β1 subunit in rat skeletal muscle is selectively associated with the tetrodotoxin α subunit isoform

    Neuron

    (1993)
  • A.N. Akopian et al.

    A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons

    Nature

    (1996)
  • P.A. Anderson et al.

    Deduced amino acid sequence of a putative sodium channel from the scyphozoan jellyfishCyanea capillata

    Proc. Natl. Acad. Sci. USA

    (1993)
  • W.J. Bailey et al.

    Phylogenetic reconstruction of vertebrateHox

    Mol. Biol. Evol.

    (1997)
  • S.M. Belcher et al.

    Cloning of a sodium channel alpha subunit from rabbit Schwann cells

    Proc. Natl. Acad. Sci. USA

    (1995)
  • P.B. Bennett et al.

    Molecular mechanism for an inherited cardiac arrhythmia

    Nature

    (1995)
  • D.E. Bulman

    Phenotype variation and newcomers in ion channel disorders

    Hum. Mol. Genet.

    (1997)
  • D.L. Burgess et al.

    Mutation of a new sodium channel gene,Scn8a,

    Nat. Genet.

    (1995)
  • S.C. Cannon et al.

    Sodium channel inactivation is impaired in equine hyperkalemic periodicparalysis

    J. Neurophysiol.

    (1995)
  • Cited by (176)

    • Crystal structure analysis, Hirshfeld surface analysis, spectral investigations (FT-IR, FT-R), DFT calculations, ADMET studies and molecular docking of 3H-Methyl-1H-pyrazole-1-carboxamide (3MPC)

      2022, Journal of the Indian Chemical Society
      Citation Excerpt :

      The membrane potentials of Nav channels switch between closed, open, and inactivated states [2]. SCNXA genes encode nine subtypes (Nav1.1 to 1.9, respectively) [3,4]. Nav1.1–Nav1.3 and Nav1.6 are the most common subtypes of the human central nervous system, Nav1.7–1.9 in the peripheral nervous system, Nav1.5 in the heart, and Nav1.4 in skeletal muscle.

    • Normal audiogram but poor sensitivity to brief sounds in mice with compromised voltage-gated sodium channels (Scn8a <sup>medJ</sup> )

      2019, Hearing Research
      Citation Excerpt :

      These channels are encoded by at least 10 genes, and several modifications of those genes in rodents have been used to explore the consequences of pinpoint mutations of this complex molecule (e.g., Caldwell et al., 2000; Mackenzie et al., 2009). The Scn8amedJ mutation is one such mutation; it reduces Scn8a voltage-gated sodium channels to 10% of their wildtype levels and causes abnormal conduction times, tremors, and motor weakness (Caldwell et al., 2000; Chen et al., 2009; Plummer and Meisler, 1999). In addition to the obvious motor abnormalities, the Scn8amedJ mutation may also affect sensory systems.

    View all citing articles on Scopus

    B. RudyP. Seeburg

    1

    Current address: Department of Genetics, Duke University Medical Center, Durham, NC 27710.

    2

    To whom correspondence should be addressed at Department of Human Genetics, Medical Science II, M4708, University of Michigan Medical School, Ann Arbor, MI 48109-0618. Telephone: (734) 763-1053. Fax: (734) 763-9691. E-mail:[email protected].

    View full text