ArticleCellular and molecular life sciences : CMLS2015
MEK1 transduces the prion protein N2 fragment antioxidant effects.
Article in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Cellular prion protein and its derived peptides: multifaceted roles in neurodegenerative diseases and potential as biomarkers.Cell & bioscience · 2026Review
- Prion Protein Endoproteolysis: Cleavage Sites, Mechanisms and Connections to Prion Disease.Journal of neurochemistry · 2025Review
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Prion Protein: The Molecule of Many Forms and Faces.International journal of molecular sciences · 2022Review
- β-Cleavage of the prion protein in the human eye: Implications for the spread of infectious prions and human ocular disorders.Experimental eye research · 2021Article
- Biological Functions of the Intrinsically Disordered N-Terminal Domain of the Prion Protein: A Possible Role of Liquid-Liquid Phase Separation.Biomolecules · 2021Review
- The Role of Cellular Prion Protein in Promoting Stemness and Differentiation in Cancer.Cancers · 2021Review
- Reduced SOD2 expression does not influence prion disease course or pathology in mice.PloS one · 2021Article
- Prions and prion diseases: Insights from the eye.Experimental eye research · 2020Review
- Show Me Your Friends and I Tell You Who You Are: The Many Facets of Prion Protein in Stroke.Cells · 2020Review
- Prion protein N1 cleavage peptides stimulate microglial interaction with surrounding cells.Scientific reports · 2020Article
- Prion Protein in Glioblastoma Multiforme.International journal of molecular sciences · 2019Review
- Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression.Cellular and molecular life sciences : CMLS · 2018Article
- Stress Resilience of Spermatozoa and Blood Mononuclear Cells without Prion Protein.Frontiers in molecular biosciences · 2018Article
- Prion protein facilitates retinal iron uptake and is cleaved at the β-site: Implications for retinal iron homeostasis in prion disorders.Scientific reports · 2017Article
- Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017Review
- Endoproteolytic cleavage as a molecular switch regulating and diversifying prion protein function.Neural regeneration research · 2016Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The prion protein (PrP(C)) when mis-folded is causally linked with a group of fatal neurodegenerative diseases called transmissible spongiform encephalopathies or prion diseases. PrP(C) normal function is still incompletely defined with such investigations complicated by PrP(C) post-translational modifications, such as internal cleavage, which feasibly could change, activate, or deactivate the function of this protein. Oxidative stress induces β-cleavage and the N-terminal product of this cleavage event, N2, demonstrates a cellular protective response against oxidative stress. The mechanisms by which N2 mediates cellular antioxidant protection were investigated within an in vitro cell model. N2 protection was regulated by copper binding to the octarepeat domain, directing the route of internalisation, which stimulated MEK1 signalling. Precise membrane interactions of N2, determined by copper saturation, and involving both the copper-co-ordinating octarepeat region and the structure conferred upon the N-terminal polybasic region by the proline motif, were essential for the correct engagement of this pathway. The phenomenon of PrP(C) post-translational modification, such as cleavage and copper co-ordination, as a molecular "switch" for activation or deactivation of certain functions provides new insight into the apparent multi-functionality of PrP(C).
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