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A mostrar 1 - 18 resultados de 18 para a pesquisa '(("specific app reconstitution") OR ("specific app reconstruction"))', tempo de pesquisa: 0.05seg Refinar resultados
  1. 1
    APP deficiency did not affect the mRNA level of <i>Scn8a</i> in cerebellar PCs.

    APP deficiency did not affect the mRNA level of <i>Scn8a</i> in cerebellar PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  2. 2
    Source data and statistical details for figures.

    Source data and statistical details for figures. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  3. 3
    L7 promoter-driven Cre recombinase expression is restricted to PCs in the cerebellar cortex.

    L7 promoter-driven Cre recombinase expression is restricted to PCs in the cerebellar cortex. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  4. 4
    Nav1.6 mediated the deficits of PC firing and motor function in APP-null mice.

    Nav1.6 mediated the deficits of PC firing and motor function in APP-null mice. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  5. 5
    Raw images for blots.

    Raw images for blots. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  6. 6
    Exogenous APP expression restored the Nav1.6 currents and ameliorated the abnormalities in the firing patterns of PCs of APP-null mice.

    Exogenous APP expression restored the Nav1.6 currents and ameliorated the abnormalities in the firing patterns of PCs of APP-null mice. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  7. 7
    Antibody validation for Nav1.6 and Nav1.1-EGFP in transfected HEK293 cells.

    Antibody validation for Nav1.6 and Nav1.1-EGFP in transfected HEK293 cells. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  8. 8
    xxx.

    xxx. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  9. 9
    APP deficiency does not alter PC development or induce degeneration.

    APP deficiency does not alter PC development or induce degeneration. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  10. 10
    APP deficiency selectively reduces Nav1.6-mediated Na<sup>+</sup> currents in cerebellar PCs.

    APP deficiency selectively reduces Nav1.6-mediated Na<sup>+</sup> currents in cerebellar PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  11. 11
    Nav1.6 Mediates most of the persistent and resurgent sodium currents in cerebellar PCs.

    Nav1.6 Mediates most of the persistent and resurgent sodium currents in cerebellar PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  12. 12
    APP-null mice exhibit motor function deficits.

    APP-null mice exhibit motor function deficits. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  13. 13
    Exogenous amyloid precursor protein (APP) expression restored the defects of the sIPSCs evoked by Nav1.6-mediated Purkenji cell inputs in APP-null mice.

    Exogenous amyloid precursor protein (APP) expression restored the defects of the sIPSCs evoked by Nav1.6-mediated Purkenji cell inputs in APP-null mice. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  14. 14
    Cerebellar Purkinje cell (PC)-specific amyloid precursor protein (APP) expression modulates motor function.

    Cerebellar Purkinje cell (PC)-specific amyloid precursor protein (APP) expression modulates motor function. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  15. 15
    PoTX potentiates persistent sodium currents in APP-null PCs.

    PoTX potentiates persistent sodium currents in APP-null PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  16. 16
    Validation of Nav1.6 and Nav1.1 contributions to sodium currents in PCs.

    Validation of Nav1.6 and Nav1.1 contributions to sodium currents in PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  17. 17
    Full-length APP is required for the rescue of motor deficit in APP-null mice.

    Full-length APP is required for the rescue of motor deficit in APP-null mice. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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  18. 18
    APP deficiency impairs the normal firing patterns of PCs.

    APP deficiency impairs the normal firing patterns of PCs. Por Miao-Jin Ji (22676552)

    Publicado em 2025
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