Matches in SemOpenAlex for { <https://semopenalex.org/work/W3135370494> ?p ?o ?g. }
- W3135370494 abstract "Abstract Neurons in human Alzheimer’s disease acquire phenotypes that are also present in various cancers, including over-stabilization of the cytoskeleton, nuclear pleomorphism, decondensation of constitutive heterochromatin, and aberrant activation of the cell cycle. Unlike in cancer, in which cell cycle activation drives tumor formation, activation of the cell cycle in post-mitotic neurons is sufficient to induce neuronal death. Multiple lines of evidence suggest that abortive cell cycle activation is a consequence of pathogenic forms of tau, a protein that drives neurodegeneration in Alzheimer’s disease and related “tauopathies.” We have combined network analysis of human Alzheimer’s disease and mouse tauopathy with mechanistic studies in Drosophila to discover that pathogenic forms of tau drive abortive cell cycle activation by disrupting the cellular program that maintains neuronal identity. Mechanistically, we identify Moesin, a prognostic biomarker for cancer and mediator of the epithelial-mesenchymal transition (EMT), as a major effector of tau-induced neurotoxicity. We find that aberrant activation of Moesin in neurons acts through the actin cytoskeleton to dysregulate the cellular program that maintains neuronal identity. Our study identifies mechanistic parallels between tauopathy and cancer and sets the stage for novel therapeutic approaches." @default.
- W3135370494 created "2021-03-15" @default.
- W3135370494 creator A5044174930 @default.
- W3135370494 creator A5069457764 @default.
- W3135370494 creator A5073198310 @default.
- W3135370494 creator A5085826986 @default.
- W3135370494 creator A5086377310 @default.
- W3135370494 date "2021-03-07" @default.
- W3135370494 modified "2023-10-16" @default.
- W3135370494 title "Pathogenic tau disrupts the cellular program that maintains neuronal identity" @default.
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- W3135370494 doi "https://doi.org/10.1101/2021.03.05.434166" @default.