Abstract
Expression of the type II voltage-dependent sodium channel gene is restricted to neurons by a silencer element active in nonneuronal cells. We have cloned cDNA coding for a transcription factor (REST) that binds to this silencer element. Expression of a recombinant REST protein confers the ability to silence type II reporter genes in neuronal cell types lacking the native REST protein, whereas expression of a dominant negative form of REST in nonneuronal cells relieves silencing mediated by the native protein. REST transcripts in developing mouse embryos are detected ubiquitously outside of the nervous system. We propose that expression of the type II sodium channel gene in neurons reflects a default pathway that is blocked in nonneuronal cells by the presence of REST.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Cell Differentiation
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Cell Nucleus / metabolism
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Cloning, Molecular
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Embryonic and Fetal Development
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Gene Expression Regulation*
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In Situ Hybridization
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Mice
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Molecular Sequence Data
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Nervous System / embryology
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Nervous System / metabolism*
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Neurons / metabolism*
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Organ Specificity
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Recombinant Proteins / biosynthesis
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Recombinant Proteins / metabolism
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Repressor Proteins / biosynthesis*
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Repressor Proteins / genetics
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Repressor Proteins / metabolism
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Saccharomyces cerevisiae
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Sequence Homology, Amino Acid
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Sodium Channels / biosynthesis*
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Transcription Factors / biosynthesis*
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Zinc Fingers
Substances
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RE1-silencing transcription factor
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Recombinant Proteins
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Repressor Proteins
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Sodium Channels
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Transcription Factors