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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Jun 2015.

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, SET
Papers on REST
RE1 silencing transcription factor/neuron-restrictive silencing factor regulates expansion of adult mouse subventricular zone-derived neural stem/progenitor cells in vitro.
New
Cacci et al., Roma, Italy. In J Neurosci Res, 31 Aug 2015
This study examines the RE1 silencing transcription factor (REST) in neural stem/progenitor cells isolated from the subventricular zone of adult mouse brain and provides the first extensive characterization of REST-mediated control of the cellular and molecular properties.
Transcriptional Mechanisms of Proneural Factors and REST in Regulating Neuronal Reprogramming of Astrocytes.
New
Impact
Götz et al., München, Germany. In Cell Stem Cell, 24 Jul 2015
Cultured astrocytes gradually became refractory to reprogramming, in part by the repressor REST preventing Neurog2 from binding to the NeuroD4 promoter.
IGF1R/IRS1 signaling confers pathogenic activity on breast tumor cells lacking REST.
New
Roopra et al., Madison, United States. In Mol Cell Biol, 22 Jul 2015
UNASSIGNED: Loss of RE-1 Silencing Transcription Factor (REST) occurs in 20% of breast cancers and correlates with poor patient prognosis.
SRRM4 Expression and the Loss of REST Activity May Promote the Emergence of the Neuroendocrine Phenotype in Castration-Resistant Prostate Cancer.
New
Morrissey et al., Washington, D.C., United States. In Clin Cancer Res, 12 Jul 2015
REST splicing was verified by PCR.
The Neuroprotective Effects of Ratanasampil on Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells.
New
Wu et al., Xining, China. In Oxid Med Cell Longev, Dec 2014
Furthermore, RNSP significantly reduced the H2O2-induced upregulation of 8-oxo-2'-deoxyguanosine (8-oxo-dG, the oxidative DNA damage marker) but significantly reversed the expression of repressor element-1 silencing transcription factor (REST) from H2O2 associated (100 μM) downregulation.
Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness.
New
Chow et al., Los Angeles, United States. In Sci Rep, Dec 2014
RE1-Silencing Transcription factor (REST) has a well-established role in regulating transcription of genes important for neuronal development.
The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation.
New
Impact
Kanduri et al., Göteborg, Sweden. In Cancer Cell, Dec 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.
New
Impact
Yankner et al., Boston, United States. In Nature, Apr 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.
HOTAIR: a cancer-related long non-coding RNA.
Review
Zhang et al., In Neoplasma, 2013
Recent studies revealed HOX transcript antisense RNA, a lncRNA with regulatory functions of transcription, could bind PRC2 and LSD1/CoREST/REST complexes and direct to the specific gene sites, resulted in H3K27 methylation and H3K4 demethylation and ultimately gene silencing.
Expression and function of the dense-core vesicle membranes are governed by the transcription repressor REST.
Review
Meldolesi et al., Castellana Grotte, Italy. In Febs Lett, 2013
REST, the transcription repressor expressed at high levels in non-neural and at very low levels in neural cells, was found to regulate the genes encoding almost all the proteins of both the core and the membrane of the dense-core vesicles, including the transporter for catecholamines and the SNAREs for their exocytosis.
The role of the CoREST/REST repressor complex in herpes simplex virus 1 productive infection and in latency.
Review
Roizman et al., Chicago, United States. In Viruses, 2013
REST is a key component of the HDAC1 or 2, CoREST, LSD1, REST (HCLR) repressor complex.
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.
Multiple Aspects of Gene Dysregulation in Huntington's Disease.
Review
Caboche et al., Paris, France. In Front Neurol, 2012
Another key mechanism described so far, is an alteration of cytoplasmic retention of the transcriptional repressor REST, which is normally associated with wild-type Htt.
Role of NRSF/REST in the regulation of cardiac gene expression and function.
Review
Kuwahara, Kyoto, Japan. In Circ J, 2012
Investigation of the transcriptional regulation of cardiac genes revealed a transcriptional repressor, neuron-restrictive silencer factor (NRSF), also called repressor element-1 silencing factor (REST), to be an important regulator of multiple fetal cardiac genes.
Microcephaly gene links trithorax and REST/NRSF to control neural stem cell proliferation and differentiation.
Impact
Walsh et al., Boston, United States. In Cell, 2012
ZNF335 is a component of a vertebrate-specific, trithorax H3K4-methylation complex, directly regulating REST/NRSF, a master regulator of neural gene expression and cell fate, as well as other essential neural-specific genes.
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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