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REST: A mammalian silencer protein that restricts sodium channel gene expression to neurons
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.
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“In nonneuronal cells and neural stem cells (NSCs), the neuronal gene expression program is suppressed by the action of the repressor element 1 (RE1) silencing transcription factor (REST) complex (Chong et al. 1995;Schoenherr and Anderson 1995).”
From Intronic miR-26b controls neuronal differentiation by repressing its host transcript,ctdsp2 (2012) · cites this paper as Chong et al. 1995
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Metadata
- Authors
- Chong, J. A., Tapia-Ramirez, J., Kim, S., Toledo-Aral, J. J., Zheng, Y., Boutros, M. C., Altshuller, Y. M., Frohman, M. A., Kraner, S. D., & Mandel, G.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1995-03
- Volume
- 80
- Issue
- 6
- Pages
- 949-957
- ISSN
- 0092-8674
- Cited by
- 967
- References
- 1
- Language
- en
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