ArticleCellular and molecular life sciences : CMLS2018
Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression.
Article in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Targeting dormant cancer cells: ferroptosis as a precision therapeutic strategy.Cellular & molecular biology letters · 2026Review
- Pterostilbene Induces Apoptosis in Awakening Quiescent Prostate Cancer Cells by Upregulating C/EBP-β-Mediated SOD2 Transcription.International journal of biological sciences · 2025Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Sirtuins and redox signaling interplay in neurogenesis, neurodegenerative diseases, and neural cell reprogramming.Frontiers in neuroscience · 2023Review
- Prion Protein: The Molecule of Many Forms and Faces.International journal of molecular sciences · 2022Review
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Review
- Neuroprotective effect and potential of cellular prion protein and its cleavage products for treatment of neurodegenerative disorders part I. a literature review.Expert review of neurotherapeutics · 2021Review
- Biological Functions of the Intrinsically Disordered N-Terminal Domain of the Prion Protein: A Possible Role of Liquid-Liquid Phase Separation.Biomolecules · 2021Review
- Disordered structure and flexible roles: using the prion protein N1 fragment for neuroprotective and regenerative therapy.Neural regeneration research · 2021Article
- Effects of Different Doses of Calcium on the Mitochondrial Apoptotic Pathway and Rho/ROCK Signaling Pathway in the Bone of Fluorosis Rats.Biological trace element research · 2021Article
- Naringin Supplementation during Pregnancy Induces Sex and Region-Specific Alterations in the Offspring's Brain Redox Status.International journal of environmental research and public health · 2021Article
- Cellular prion protein dysfunction in a prototypical inherited metabolic myopathy.Cellular and molecular life sciences : CMLS · 2021Article
- Reduced SOD2 expression does not influence prion disease course or pathology in mice.PloS one · 2021Article
- Show Me Your Friends and I Tell You Who You Are: The Many Facets of Prion Protein in Stroke.Cells · 2020Review
- Prion Protein in Stem Cells: A Lipid Raft Component Involved in the Cellular Differentiation Process.International journal of molecular sciences · 2020Review
- Prion protein N1 cleavage peptides stimulate microglial interaction with surrounding cells.Scientific reports · 2020Article
- Oxidative DNA Damage Signalling in Neural Stem Cells in Alzheimer's Disease.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Neurogenesis continues in the post-developmental brain throughout life. The ability to stimulate the production of new neurones requires both quiescent and actively proliferating pools of neural stem cells (NSCs). Actively proliferating NSCs ensure that neurogenic demand can be met, whilst the quiescent pool makes certain NSC reserves do not become depleted. The processes preserving the NSC quiescent pool are only just beginning to be defined. Herein, we identify a switch between NSC proliferation and quiescence through changing intracellular redox signalling. We show that N-terminal post-translational cleavage products of the prion protein (PrP) induce a quiescent state, halting NSC cellular growth, migration, and neurite outgrowth. Quiescence is initiated by the PrP cleavage products through reducing intracellular levels of reactive oxygen species. First, inhibition of redox signalling results in increased mitochondrial fission, which rapidly signals quiescence. Thereafter, quiescence is maintained through downstream increases in the expression and activity of superoxide dismutase-2 that reduces mitochondrial superoxide. We further observe that PrP is predominantly cleaved in quiescent NSCs indicating a homeostatic role for this cascade. Our findings provide new insight into the regulation of NSC quiescence, which potentially could influence brain health throughout adult life.
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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.