ArticleFrontiers in molecular neuroscience2017
Downregulation of the Repressor Element 1-Silencing Transcription Factor (REST) Is Associated with Akt-mTOR and Wnt-β-Catenin Signaling in Prion Diseases Models.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- CoREST3 exhibits isoform specific expression in Alzheimer's disease and regulation of HDAC2.BMC biology · 2025Article
- Lipopolysaccharides fromJournal of Alzheimer's disease : JAD · 2025Article
- Article
- PHB2 Alleviates Neurotoxicity of Prion Peptide PrPInternational journal of molecular sciences · 2023Article
- Cardiolipin externalization mediates prion protein (PrP) peptide 106-126-associated mitophagy and mitochondrial dysfunction.Frontiers in molecular neuroscience · 2023Article
- Human iPSC-Derived Neurons as A Platform for Deciphering the Mechanisms behind Brain Aging.Biomedicines · 2021Review
- Comprehensive Analysis of REST/NRSF Gene in Glioma and Its ceRNA Network Identification.Frontiers in medicine · 2021Article
- 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
- Article
- Regulation of MicroRNAs-Mediated Autophagic Flux: A New Regulatory Avenue for Neurodegenerative Diseases With Focus on Prion Diseases.Frontiers in aging neuroscience · 2018Review
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are a group of infectious diseases characterized by multiple neuropathological changes, yet the mechanisms that preserve function and protect against prion-associated neurodegeneration are still unclear. We previously reported that the repressor element 1-silencing transcription factor (REST) alleviates neurotoxic prion peptide (PrP106-126)-induced toxicity in primary neurons. Here we confirmed the findings of the
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Registered trials
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