Molecular studies of two voltage-dependent sodium channels expressed in the nervous system

S. Kraner, K. Dains, Gail Mandel

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The action potential in most excitable cells is generated in response to the rapid opening and closing of the voltage-sensitive sodium channel. In vertebrate skeletal muscle and brain this channel consists of a large, glycosylated alpha subunit (approximately 260 kDa) and one or two smaller beta subunits (approximately 35-40 kDa). The alpha subunit is encoded by a large multi-gene family, the members of which are expressed in a tissue-specific manner. Two of the genes, encoding the type I and II sodium channels, are expressed at high levels within the central nervous system. We have performed experiments showing that genetic components responsible for neural specificity of these sodium channel genes is located upstream of the promoters. In particular, negatively-acting elements have been identified which repress sodium channel gene expression in non-neural cell lines. Identification of the proteins which mediate neural-specific expression should prove useful for genetic manipulation of sodium channel expression in vivo, and for providing a molecular framework for understanding neural-specific expression in general.

Original languageEnglish (US)
Pages (from-to)27-30
Number of pages4
JournalBiomedical Research
Volume12
Issue numberSUPPL. 2
StatePublished - 1991
Externally publishedYes

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Sodium Channels
Neurology
Nervous System
Electric potential
Genes
Gene encoding
Gene expression
Action Potentials
Muscle
Vertebrates
Brain
Skeletal Muscle
Central Nervous System
Cells
Tissue
Gene Expression
Cell Line
Proteins
Experiments

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Molecular studies of two voltage-dependent sodium channels expressed in the nervous system. / Kraner, S.; Dains, K.; Mandel, Gail.

In: Biomedical Research, Vol. 12, No. SUPPL. 2, 1991, p. 27-30.

Research output: Contribution to journalArticle

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