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Altered steady state and activity-dependent de novo protein expression in fragile X syndrome

Author

Listed:
  • Heather Bowling

    (New York University)

  • Aditi Bhattacharya

    (New York University
    Institute for Stem Cell Biology and Regenerative Medicine)

  • Guoan Zhang

    (New York University School of Medicine)

  • Danyal Alam

    (New York University)

  • Joseph Z. Lebowitz

    (New York University)

  • Nathaniel Bohm-Levine

    (New York University)

  • Derek Lin

    (New York University)

  • Priyangvada Singha

    (Institute for Stem Cell Biology and Regenerative Medicine)

  • Maggie Mamcarz

    (New York University)

  • Rosemary Puckett

    (New York University)

  • Lili Zhou

    (Rush University Medical Center)

  • Sameer Aryal

    (New York University
    New York University School of Medicine)

  • Kevin Sharp

    (Rush University Medical Center)

  • Kent Kirshenbaum

    (New York University)

  • Elizabeth Berry-Kravis

    (Rush University Medical Center
    Rush University Medical Center)

  • Thomas A. Neubert

    (New York University School of Medicine)

  • Eric Klann

    (New York University
    New York University School of Medicine)

Abstract

Whether fragile X mental retardation protein (FMRP) target mRNAs and neuronal activity contributing to elevated basal neuronal protein synthesis in fragile X syndrome (FXS) is unclear. Our proteomic experiments reveal that the de novo translational profile in FXS model mice is altered at steady state and in response to metabotropic glutamate receptor (mGluR) stimulation, but the proteins expressed differ under these conditions. Several altered proteins, including Hexokinase 1 and Ras, also are expressed in the blood of FXS model mice and pharmacological treatments previously reported to ameliorate phenotypes modify their abundance in blood. In addition, plasma levels of Hexokinase 1 and Ras differ between FXS patients and healthy volunteers. Our data suggest that brain-based de novo proteomics in FXS model mice can be used to find altered expression of proteins in blood that could serve as disease-state biomarkers in individuals with FXS.

Suggested Citation

  • Heather Bowling & Aditi Bhattacharya & Guoan Zhang & Danyal Alam & Joseph Z. Lebowitz & Nathaniel Bohm-Levine & Derek Lin & Priyangvada Singha & Maggie Mamcarz & Rosemary Puckett & Lili Zhou & Sameer , 2019. "Altered steady state and activity-dependent de novo protein expression in fragile X syndrome," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09553-8
    DOI: 10.1038/s41467-019-09553-8
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    Cited by:

    1. Sang S. Seo & Susana R. Louros & Natasha Anstey & Miguel A. Gonzalez-Lozano & Callista B. Harper & Nicholas C. Verity & Owen Dando & Sophie R. Thomson & Jennifer C. Darnell & Peter C. Kind & Ka Wan Li, 2022. "Excess ribosomal protein production unbalances translation in a model of Fragile X Syndrome," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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