ArticleOncotarget2016
REST alleviates neurotoxic prion peptide-induced synaptic abnormalities, neurofibrillary degeneration and neuronal death partially via LRP6-mediated Wnt-β-catenin signaling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Complexity of PEDF multifunctional signaling in retinal development and diseases.Communications biology · 2026Article
- Tamoxifen induces partial neuroprotection against manganese toxicity in the dopaminergic REST-deleted male mice.Neurotoxicology · 2025Article
- Calcium-dependent serine-threonine phosphatase and autophagy inactivation mediated by Baicalein attenuates prion protein-mediated neuronal cell damage.BMC complementary medicine and therapies · 2025Article
- Lipopolysaccharides fromJournal of Alzheimer's disease : JAD · 2025Article
- SARM1 participates in axonal degeneration and mitochondrial dysfunction in prion disease.Neural regeneration research · 2022Article
- REST/NRSF deficiency impairs autophagy and leads to cellular senescence in neurons.Aging cell · 2021Article
- LRP6 mediated signal transduction pathway triggered by tissue plasminogen activator acts through lipid rafts in neuroblastoma cells.Journal of cell communication and signaling · 2020Article
- Possible mechanisms of lycopene amelioration of learning and memory impairment in rats with vascular dementia.Neural regeneration research · 2020Article
- OPA1 overexpression ameliorates mitochondrial cristae remodeling, mitochondrial dysfunction, and neuronal apoptosis in prion diseases.Cell death & disease · 2019Article
- Combinatory FK506 and Minocycline Treatment Alleviates Prion-Induced Neurodegenerative Events via Caspase-Mediated MAPK-NRF2 Pathway.International journal of molecular sciences · 2019Article
- Chronic Metabolic Derangement-Induced Cognitive Deficits and Neurotoxicity Are Associated with REST Inactivation.Molecular neurobiology · 2019Article
- Prion protein is essential for the RE1 silencing transcription factor (REST)-dependent developmental switch in synaptic NMDA receptors.Cell death & disease · 2018Article
- Wnts Promote Synaptic Assembly Through T-Cell Specific Transcription Factors inFrontiers in molecular neuroscience · 2018Article
- Regulation of MicroRNAs-Mediated Autophagic Flux: A New Regulatory Avenue for Neurodegenerative Diseases With Focus on Prion Diseases.Frontiers in aging neuroscience · 2018Review
- PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling.CNS neuroscience & therapeutics · 2017Article
- Early Minocycline and Late FK506 Treatment Improves Survival and Alleviates Neuroinflammation, Neurodegeneration, and Behavioral Deficits in Prion-Infected Hamsters.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Article
- Downregulation of the Repressor Element 1-Silencing Transcription Factor (REST) Is Associated with Akt-mTOR and Wnt-β-Catenin Signaling in Prion Diseases Models.Frontiers in molecular neuroscience · 2017Article
- The Role of Unfolded Protein Response and Mitogen-Activated Protein Kinase Signaling in Neurodegenerative Diseases with Special Focus on Prion Diseases.Frontiers in aging neuroscience · 2017Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are a group of infectious neurodegenerative diseases characterized by multiple neuropathological hallmarks including synaptic damage, spongiform degeneration and neuronal death. The factors and mechanisms that maintain cellular morphological integrity and protect against neurodegeneration in prion diseases are still unclear. Here we report that after stimulation with the neurotoxic PrP106-126 fragment in primary cortical neurons, REST translocates from the cytoplasm to the nucleus and protects neurons from harmful effects of PrP106-126. Overexpression of REST reduces pathological damage and abnormal biochemical alterations of neurons induced by PrP106-126 and maintains neuronal viability by stabilizing the level of pro-survival protein FOXO1 and inhibiting the permeability of the mitochondrial outer membrane, release of cytochrome c from mitochondria to cytoplasm and the activation of Capase3. Conversely, knockdown of REST exacerbates morphological damage and inhibits the expression of FOXO1. Additionally, by overexpression or knockdown of LRP6, we further show that LRP6-mediated Wnt-β-catenin signaling partly regulates the expression of REST. Collectively, we demonstrate for the first time novel neuroprotective function of REST in prion diseases and hypothesise that the LRP6-Wnt-β-catenin/REST signaling plays critical and collaborative roles in neuroprotection. This signaling of neuronal survival regulation could be explored as a viable therapeutic target for prion diseases and associated neurodegenerative diseases.
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