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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 21 May 2016.

RE1-silencing transcription factor

REST, NRSF, neuron-restrictive silencer factor
This gene encodes a transcriptional repressor that represses neuronal genes in non-neuronal tissues. It is a member of the Kruppel-type zinc finger transcription factor family. It represses transcription by binding a DNA sequence element called the neuron-restrictive silencer element. The protein is also found in undifferentiated neuronal progenitor cells and it is thought that this repressor may act as a master negative regular of neurogenesis. Alternatively spliced transcript variants have been described [provided by RefSeq, Jul 2010] (from NCBI)
Top mentioned proteins: CAN, Histone, V1a, CoREST, ACID
Papers on REST
KCC2 rescues functional deficits in human neurons derived from patients with Rett syndrome.
New
Chen et al., Los Angeles, United States. In Proc Natl Acad Sci U S A, Feb 2016
We further identified that RE1-silencing transcriptional factor, REST, a neuronal gene repressor, mediates the MeCP2 regulation of KCC2.
Brain REST/NRSF Is Not Only a Silent Repressor but Also an Active Protector.
New
Zhang et al., Chongqing, China. In Mol Neurobiol, Feb 2016
Repressor element-1 binding transcription factor (REST), or neuron-restrictive silencer factor (NRSF), has been shown to be an important regulator for the establishment of neuronal specificity.
miR-124-9-9* potentiates Ascl1-induced reprogramming of cultured Müller glia.
New
Reh et al., Seattle, United States. In Glia, Feb 2016
Analysis of the miR-124-9-9* treated glial cells showed a reduction in the level of Ctdsp1 and Ptbp1, indicating a critical role for the REST pathway in the repression of neuronal genes in Müller glia.
Selective repression of gene expression in neuropathic pain by the neuron-restrictive silencing factor/repressor element-1 silencing transcription (NRSF/REST).
Review
New
Cave et al., White Plains, United States. In Neurosci Lett, Jan 2016
In this review, we discuss recent evidence that the DNA-binding protein neuron-restrictive silencing factor/repressor element-1 silencing transcription factor (NRSF/REST) is an important component in the development and maintenance of neuropathic pain through its role as a transcriptional regulator for a select subset of genes that it normally represses during development.
Mutations in the transcriptional repressor REST predispose to Wilms tumor.
New
Impact
Rahman et al., Houston, United States. In Nat Genet, Dec 2015
Here we describe 11 different inactivating mutations in the REST gene (encoding RE1-silencing transcription factor) in four familial Wilms tumor pedigrees and nine non-familial cases.
Give it a REST!
New
Angeles Marques et al., Edinburgh, United Kingdom. In Elife, Dec 2015
The REST protein helps to prevent the premature activation of genes that are only expressed in mature neurons, and is now found to protect the genome of neural progenitor cells.
The REST remodeling complex protects genomic integrity during embryonic neurogenesis.
New
Mandel et al., Portland, United States. In Elife, Dec 2015
The timely transition from neural progenitor to post-mitotic neuron requires down-regulation and loss of the neuronal transcriptional repressor, REST.
Schizophrenia: Evidence implicating hippocampal GluN2B protein and REST epigenetics in psychosis pathophysiology.
Review
New
Zukin et al., Dallas, United States. In Neuroscience, Dec 2015
We interpret these observations to implicate a reduction in the influence of a ubiquitous gene repressor, repressor element-1 silencing transcription factor (REST) in psychosis; REST is involved in the age-related maturation of the NMDA receptor from GluN2B- to GluN2A-containing NMDA receptors through epigenetic remodeling.
Transcriptional Mechanisms of Proneural Factors and REST in Regulating Neuronal Reprogramming of Astrocytes.
New
Impact
Götz et al., München, Germany. In Cell Stem Cell, Aug 2015
Cultured astrocytes gradually became refractory to reprogramming, in part by the repressor REST preventing Neurog2 from binding to the NeuroD4 promoter.
The Transcription Repressor REST in Adult Neurons: Physiology, Pathology, and Diseases(1,2,3).
Review
New
Meldolesi et al., Genova, Italy. In Eneuro, Jul 2015
REST [RE1-silencing transcription factor (also called neuron-restrictive silencer factor)] is known to repress thousands of possible target genes, many of which are neuron specific.
NRSF: an angel or a devil in neurogenesis and neurological diseases.
Review
New
Yang et al., Beijing, China. In J Mol Neurosci, May 2015
The neuron-restrictive silencer factor (NRSF) a transcriptional regulator that function as a hub that coordinately regulates multiple aspects of neurogenesis, orchestrates neural differentiation, and preserves the unique neural phenotype.
RE-1 silencing transcription factor (REST): a regulator of neuronal development and neuronal/endocrine function.
Review
Rössler et al., Homburg, Germany. In Cell Tissue Res, 2015
RE-1 silencing transcription factor (REST) is a transcriptional repressor that has been proposed to function as a master negative regulator of neurogenesis, as REST target genes encode neuronal receptors, ion channels, neuropeptides and synaptic proteins.
The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation.
Impact
Kanduri et al., Göteborg, Sweden. In Cancer Cell, 2014
NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST.
REST and stress resistance in ageing and Alzheimer's disease.
Impact
Yankner et al., Boston, United States. In Nature, 2014
Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons.
Direct conversion of fibroblasts to neurons by reprogramming PTB-regulated microRNA circuits.
Impact
Fu et al., Wuhan, China. In Cell, 2013
A key event during neuronal induction is the relief of PTB-mediated blockage of microRNA action on multiple components of the REST complex, thereby derepressing a large array of neuronal genes, including miR-124 and multiple neuronal-specific transcription factors, in nonneuronal cells.
REST regulates the pool size of the different neural lineages by restricting the generation of neurons and oligodendrocytes from neural stem/progenitor cells.
GeneRIF
Ballas et al., Stony Brook, United States. In Development, 2012
central role for REST during neural development in promoting neural stem/progenitor cell self-renewal while restricting the generation and maturation of neurons and oligodendrocytes
Induction of the RNA regulator LIN28A is required for the growth and pathogenesis of RESTless breast tumors.
GeneRIF
Roopra et al., Madison, United States. In Cancer Res, 2012
findings therefore show a critical role for the REST-LIN28A axis in tumor aggression and suggest a causative relationship between REST loss and tumorigenicity in vivo
The joint association of REST and NFKB1 polymorphisms on the risk of colorectal cancer.
GeneRIF
Chen et al., Hangzhou, China. In Ann Hum Genet, 2012
the present study found that mutation in the REST gene rather than the NFKB1 gene was associated with the risk of CRC.
Ubiquitination and deubiquitination of REST and its roles in cancers.
Review
GeneRIF
Bao et al., Cleveland, United States. In Febs Lett, 2012
role of REST in cancers
REST controls self-renewal and tumorigenic competence of human glioblastoma cells.
GeneRIF
Cattaneo et al., Milano, Italy. In Plos One, 2011
REST controls self-renewal and tumorigenic competence of human glioblastoma cells.
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