ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Ischemic insults derepress the gene silencer REST in neurons destined to die.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.
What it found
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Who cites it
171 citing papers in PubMed, 315 citations in OpenAlex.
- Phosphorylation by CaMKIV regulates the transcriptional repressor activity and half-life of REST/NRSF.Science advances · 2026Article
- siRNA for REST ameliorates symptoms in ALS mice and serum REST predicts disease prognosis and survival in ALS patients.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- An Alzheimer's disease-associated mutant ofmicroPublication biology · 2026Article
- Pharmacological inhibition of RE1 silencing transcription factor disrupts SOX2 expression and neurogenesis in human induced pluripotent stem cells derived neuronal models.Metabolic brain disease · 2025Article
- The Dynamic Roles of Repressor Element 1-Silencing Transcription Factor (REST): A Double-Edged Sword in Neural Health and Disease.Molecular neurobiology · 2025Review
- CoREST3 exhibits isoform specific expression in Alzheimer's disease and regulation of HDAC2.BMC biology · 2025Article
- Hydrogen Peroxide-Induced Re-Expression of Repressor Element 1-Silencing Transcription Factor Contributes to Cardiac Vagal Dysfunction in Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2025Article
- REST Is Restless in Neuronal and Non-Neuronal Virus Infections: An In Silico Analysis-Based Perspective.Viruses · 2025Review
- Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- REST in the Road Map of Brain Development.Cellular and molecular neurobiology · 2023Review
- In the fast lane: Receptor trafficking during status epilepticus.Epilepsia open · 2023Review
- Electron microscopy reveals toroidal shape of master neuronal cell differentiator REST - RE1-silencing transcription factor.Computational and structural biotechnology journal · 2023Article
- Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022Review
- Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer's disease.Molecular neurodegeneration · 2022Article
- Roles of the Neuron-Restrictive Silencer Factor in the Pathophysiological Process of the Central Nervous System.Frontiers in cell and developmental biology · 2022Review
- Knockdown of NRSF Alleviates Ischemic Brain Injury and Microvasculature Defects in Diabetic MCAO Mice.Frontiers in neurology · 2022Article
- The Genome-Wide Binding Profile for Human RE1 Silencing Transcription Factor Unveils a Unique Genetic Circuitry in Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- CSF Proteomic Alzheimer's Disease-Predictive Subtypes in Cognitively Intact Amyloid Negative Individuals.Proteomes · 2021Article
- Expression of Selected Genes Involved in Neurogenesis in the Etiopathogenesis of Depressive Disorders.Journal of personalized medicine · 2021Article
111 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
A subset of genes implicated in genetic and acquired neurological disorders encode proteins essential to neural patterning and neurogenesis. The gene silencing transcription factor neuronal repressor element-1 silencing transcription factor (REST)/neuron-restrictive silencer factor (NRSF) plays a critical role in elaboration of the neuronal phenotype. In neural progenitor and non-neural cells, REST acts by repression of a subset of neural genes important to synaptic plasticity and synaptic remodeling, including the AMPA receptor (AMPAR) subunit GluR2. Here we show that global ischemia triggers REST mRNA and protein expression. REST suppresses GluR2 promoter activity and gene expression in neurons destined to die. Because the GluR2 subunit governs AMPAR Ca2+ permeability, these changes are expected to have profound effects on neuronal survival. In keeping with this concept, acute knockdown of the REST gene by antisense administration prevents GluR2 suppression and rescues post-ischemic neurons from ischemia-induced cell death in an in vitro model. To our knowledge, our study represents the first example of ischemia-induced induction of a master transcriptional regulator gene and its protein expression critical to neural differentiation and patterning in adult neurons. Derepression of REST is likely to be an important mechanism of insult-induced neuronal death.
Indexed as
Identifiers
12657670PMC6741998W2100013751What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.