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Related Experiment Videos

Proteolysis in quaking mouse brain and spinal cord.

W W McAlhaney, N L Banik, S Greenfield

    Neurochemical Research
    |February 1, 1986
    PubMed
    Summary

    Proteolytic enzyme activity in the quaking mutant mouse central nervous system (CNS) was investigated. Results showed similar enzyme levels in mutant and normal mice, suggesting proteolysis is not the cause of hypomyelination.

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    Area of Science:

    • Neuroscience
    • Biochemistry
    • Genetics

    Background:

    • The quaking mouse is a model for hypomyelination.
    • Increased proteolytic activity has been hypothesized to contribute to hypomyelination in this mutant.

    Purpose of the Study:

    • To investigate the activity of six specific proteolytic enzymes in the central nervous system (CNS) of quaking mutant mice.
    • To determine if altered proteolytic activity is associated with the hypomyelination characteristic of the quaking mutation.

    Main Methods:

    • Assayed activity of cathepsin B-like enzyme, cathepsin D, neutral proteinase, calcium-activated neutral proteinase, prolyl endopeptidase, and diaminopeptidase II.
    • Enzyme activity was measured in whole homogenates of brain and spinal cord from quaking mutant and normal mice.

    Main Results:

    • All six assayed proteolytic enzymes exhibited similar activity levels in the CNS of quaking mutant mice compared to normal mice.
    • No significant differences in the activity of these enzymes were detected between the mutant and control groups.

    Conclusions:

    • The findings do not support a direct relationship between increased proteolytic activity and the genetic defect causing hypomyelination in quaking mice.
    • Other etiological factors should be explored to understand the pathogenesis of hypomyelination in this neurological mutant model.

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