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  • Study: Protein found to be key component in irregularly excited brain cells

    Researchers discovered that an overabundance of the tumor suppressor protein p53 in neurons can lead to impaired regulation of neuronal excitability in a mouse model of Fragile X syndrome.

    Research scientist Kwan Young Lee, left, molecular and integrative physiology professor Nien-Pei Tsai and their colleagues discovered that an overabundance of the tumor suppressor protein p53 in neurons can lead to impaired regulation of neuronal excitability in a mouse model of Fragile X syndrome.

    Photo by Steph Adams

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  • Editor’s notes:
    To reach Nien-Pei Tsai, call 217-244-5620; email nptsai@illinois.edu
    The papers “Loss of fragile X protein FMRP impairs homeostatic synaptic downscaling through tumor suppressor p53 and ubiquitin E3 ligase Nedd4-2” and “Dysregulation and restoration of homeostatic network plasticity in fragile X syndrome mice” are available online and from the U. of I. News Bureau.
    DOI: 10.1093/hmg/ddy189
    DOI: 10.1016/j.neuropharm.2018.06.011