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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 Aug 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, ACID
Papers on REST
Cohesin recruits the Esco1 acetyltransferase genome wide to repress transcription and promote cohesion in somatic cells.
Jallepalli et al., New York City, United States. In Proc Natl Acad Sci U S A, 24 Sep 2015
Here we show that Esco1 and Esco2 also differ dramatically in their interaction with chromatin, as Esco1 is recruited by cohesin to over 11,000 sites, whereas Esco2 is infrequently enriched at REST/NRSF target genes.
Resveratrol Via Sirtuin-1 Downregulates RE1-Silencing Transcription Factor (REST) Expression Preventing PCB-95-Induced Neuronal Cell Death.
Formisano et al., Napoli, Italy. In Toxicol Appl Pharmacol, 22 Sep 2015
By contrast, the RE1-silencing transcription factor (REST) is involved in the neurotoxic effects following exposure to polychlorinated biphenyl (PCB) mixture A1254.
Functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated human prostate cancer cells.
Kawabata et al., Ōsaka, Japan. In Biochem Pharmacol, 06 Sep 2015
During differentiation, Egr-1 and REST, positive and negative transcriptional regulators for Cav3.2, were upregulated and downregulated, respectively, and Egr-1 knockdown prevented the Cav3.2 overexpression.
Peripheral and central control of swallowing initiation in healthy humans.
Inoue et al., Niigata, Japan. In Physiol Behav, 04 Sep 2015
Eleven participants completed a repetitive saliva swallowing test (RSST), chewing test (CHEW), and rest period (REST).
Schizophrenia: Evidence Implicating Hippocampal GluN2B protein and REST Epigenetics in Psychosis Pathophysiology.
Suzanne Zukin et al., New York City, United States. In Neuroscience, 23 Aug 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.
Götz et al., München, Germany. In Cell Stem Cell, 02 Aug 2015
Cultured astrocytes gradually became refractory to reprogramming, in part by the repressor REST preventing Neurog2 from binding to the NeuroD4 promoter.
The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Cattaneo et al., Milano, Italy. In Plos One, 2011
REST controls self-renewal and tumorigenic competence of human glioblastoma cells.
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