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    Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice

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    Williamson_Open_Biology (1.008Mb)
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    Publication date
    2019-11-06
    Author
    Muha, V.
    Williamson, Ritchie
    Hills, R.
    McNeilly, A.D.
    McWilliams, T.G.
    Alonso, J.
    Schimpl, M.
    Leney, A.C.
    Heck, A.J.R.
    Sutherland, C.
    Read, K.D.
    McCrimmon, R.J.
    Brooks, S.P.
    van Aalten, D.M.F.
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    Keyword
    O-GlcNAcylation
    CRMP2
    Cross talk
    Cognitive function
    Rights
    © 2019 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.
    Peer-Reviewed
    Yes
    
    Metadata
    Show full item record
    Abstract
    O-GlcNAcylation is an abundant post-translational modification in the nervous system, linked to both neurodevelopmental and neurodegenerative disease. However, the mechanistic links between these phenotypes and site-specific O-GlcNAcylation remain largely unexplored. Here, we show that Ser517 O-GlcNAcylation of the microtubule-binding protein Collapsin Response Mediator Protein-2 (CRMP2) increases with age. By generating and characterizing a Crmp2S517A knock-in mouse model, we demonstrate that loss of O-GlcNAcylation leads to a small decrease in body weight and mild memory impairment, suggesting that Ser517 O-GlcNAcylation has a small but detectable impact on mouse physiology and cognitive function.
    URI
    http://hdl.handle.net/10454/17525
    Version
    Published version
    Citation
    Muha V, Williamson R, Hills R et al (2019) Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice. Open Biology. 9(11): 190192.
    Link to publisher’s version
    https://doi.org/10.1098/rsob.190192
    Type
    Article
    Collections
    Life Sciences Publications

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