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    Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic

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    Author
    Trist, BG; Hilton, JB; Hare, DJ; Crouch, PJ; Double, KL
    Date
    2020-11-19
    Source Title
    Angewandte Chemie International Edition
    Publisher
    WILEY-V C H VERLAG GMBH
    University of Melbourne Author/s
    Crouch, Peter; Hilton, James; Hare, Dominic
    Affiliation
    Pharmacology and Therapeutics
    School of BioSciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Trist, B. G., Hilton, J. B., Hare, D. J., Crouch, P. J. & Double, K. L. (2020). Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic. ANGEWANDTE CHEMIE-INTERNATIONAL EDITION, https://doi.org/10.1002/anie.202000451.
    Access Status
    Access this item via the Open Access location
    URI
    http://hdl.handle.net/11343/254164
    DOI
    10.1002/anie.202000451
    Open Access URL
    http://doi.org/10.1002/anie.202000451
    Abstract
    Cu/Zn superoxide dismutase (SOD1) is a frontline antioxidant enzyme catalysing superoxide breakdown and is important for most forms of eukaryotic life. The evolution of aerobic respiration by mitochondria increased cellular production of superoxide, resulting in an increased reliance upon SOD1. Consistent with the importance of SOD1 for cellular health, many human diseases of the central nervous system involve perturbations in SOD1 biology. But far from providing a simple demonstration of how disease arises from SOD1 loss-of-function, attempts to elucidate pathways by which atypical SOD1 biology leads to neurodegeneration have revealed unexpectedly complex molecular characteristics delineating healthy, functional SOD1 protein from that which likely contributes to central nervous system disease. This review summarises current understanding of SOD1 biology from SOD1 genetics through to protein function and stability.

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