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    SUMO-1 conjugation blocks beta-amyloid-induced astrocyte reactivity.

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    Publication date
    2013-06
    Author
    Hoppe, J.B.
    Rattray, Marcus
    Tu, H.
    Salbego, C.G.
    Cimarosti, H.
    Keyword
    Alzheimer's disease; Beta-amyloid peptide; c-Jun N-terminal kinase; Curcumin; Reactivity; Small ubiquitin-like modifier (SUMO) conjugation
    Peer-Reviewed
    yes
    
    Metadata
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    Abstract
    Astrocyte reactivity is implicated in the neuronal loss underlying Alzheimer's disease. Curcumin has been shown to reduce astrocyte reactivity, though the exact pathways underlying these effects are incompletely understood. Here we investigated the role of the small ubiquitin-like modifier (SUMO) conjugation in mediating this effect of curcumin. In beta-amyloid (Aβ)-treated astrocytes, morphological changes and increased glial fibrillary acidic protein (GFAP) confirmed reactivity, which was accompanied by c-jun N-terminal kinase activation. Moreover, the levels of SUMO-1 conjugated proteins, as well as the conjugating enzyme, Ubc9, were decreased, with concomitant treatment with curcumin preventing these effects. Increasing SUMOylation in astrocytes, by over-expression of constitutively active SUMO-1, but not its inactive mutant, abrogated Aβ-induced increase in GFAP, suggesting astrocytes require SUMO-1 conjugation to remain non-reactive.
    URI
    http://hdl.handle.net/10454/7805
    Version
    Accepted Manuscript
    Citation
    Hoppe JB, Rattray M, Tu H, Salbego CG and Cimarosti H (2013) SUMO-1 conjugation blocks beta-amyloid-induced astrocyte reactivity. Neuroscience Letters, 546: 51-6.
    Link to publisher’s version
    http://doi.org/10.1016/j.neulet.2013.04.050
    Type
    Article
    Collections
    Life Sciences Publications

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