ArticleCNS neuroscience & therapeutics2017
PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Ischemic stroke altered the expression profiles of super enhancer RNAs in mouse brain in a sexually dimorphic manner.Experimental neurology · 2025Article
- Purine metabolism in bone marrow microenvironment inhibits hematopoietic stem cell differentiation under microgravity.Stem cell research & therapy · 2025Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- PHB2 Alleviates Neurotoxicity of Prion Peptide PrPInternational journal of molecular sciences · 2023Article
- Montelukast Induces Apoptosis-Inducing Factor-Mediated Cell Death of Lung Cancer Cells.International journal of molecular sciences · 2017Article
- PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling.CNS neuroscience & therapeutics · 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
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe proline-rich Akt substrate of 40-kDa (PRAS40) protein is a direct inhibitor of mTORC1 and an interactive linker between the Akt and mTOR pathways. The mammalian target of rapamycin (mTOR) is considered to be a central regulator of cell growth and metabolism. Several investigations have demonstrated that abnormal mTOR activity may contribute to the pathogenesis of several neurodegenerative disorders and lead to cognitive deficits.
methodsHere, we used the PrP peptide 106-126 (PrP
resultsWe have shown that, upon stress caused by PrP
conclusionPRAS40 inhibits mTORC1 hyperactivation and plays a key role in protecting cells against neurotoxic prion peptide-induced apoptosis. Thus, PRAS40 is a potential therapeutic target for prion disease.
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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.