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Study · In vitro (cells) · rat · 2012

7 results

The ADNP derived peptide, NAP modulates the tubulin pool: implication for neurotrophic and neuroprotective activities.

Oz S, Ivashko-Pachima Y, Gozes I

PloS one14 Dec 2012Cited by 70 (Europe PMC)

PMID23272107 (opens in a new tab)PMCIDPMC3522725 (opens in a new tab)DOI10.1371/journal.pone.0051458 (opens in a new tab)PepBankPUB-23272107
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Summary

Microtubules (MTs), key cytoskeletal elements in living cells, are critical for axonal transport, synaptic transmission, and maintenance of neuronal morphology. NAP (NAPVSIPQ) is a neuroprotective peptide derived from the essential activity-dependent neuroprotective protein (ADNP). In Alzheimer's disease models, NAP protects against tauopathy and cognitive decline. Here, we show that NAP treatment significantly affected the alpha tubulin tyrosination cycle in the neuronal differentiation model, rat pheochromocytoma (PC12) and in rat cortical astrocytes. The effect on tubulin tyrosination/detyrosination was coupled to increased MT network area (measured in PC12 cells), which is directly related to neurite outgrowth. Tubulin beta3, a marker for neurite outgrowth/neuronal differentiation significantly increased after NAP treatment. In rat cortical neurons, NAP doubled the area of dynamic MT invasion (Tyr-tubulin) into the neuronal growth cone periphery. NAP was previously shown to protect against zinc-induced MT/neurite destruction and neuronal death, here, in PC12 cells, NAP treatment reversed zinc-decreased tau-tubulin-MT interaction and protected against death. NAP effects on the MT pool, coupled with increased tau engagement on compromised MTs imply an important role in neuronal plasticity, protecting against free tau accumulation leading to tauopathy. With tauopathy representing a major pathological hallmark in Alzheimer's disease and related disorders, the current findings provide a mechanistic basis for further development. NAP (davunetide) is in phase 2/3 clinical trial in progressive supranuclear palsy, a disease presenting MT deficiency and tau pathology.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

7 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In rat PC12 cells, NAP significantly affected the alpha tubulin tyrosination cycle.

    In plain wordsIn cells, NAP changed the tubulin tyrosination cycle.

    Peptide
    Davunetide
    Outcome
    Direction not reportedTubulin tyrosination cycle in PC12 cells
    Study

    ratn: not reported in source

    PC12 cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that NAP treatment significantly affected the alpha tubulin tyrosination cycle in the neuronal differentiation model, rat pheochromocytoma (PC12) and in rat cortical astrocytes.
  2. 02LabIn vitro (cells)Mechanism

    In rat cortical astrocytes, NAP significantly affected the alpha tubulin tyrosination cycle.

    In plain wordsIn cells, NAP changed the tubulin tyrosination cycle in rat astrocytes.

    Peptide
    Davunetide
    Outcome
    Direction not reportedTubulin tyrosination cycle in astrocytes
    Study

    ratn: not reported in source

    Rat cortical astrocytes
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we show that NAP treatment significantly affected the alpha tubulin tyrosination cycle in the neuronal differentiation model, rat pheochromocytoma (PC12) and in rat cortical astrocytes.
  3. 03LabIn vitro (cells)Mechanism

    In PC12 cells, NAP-associated tubulin changes accompanied increased microtubule network area.

    In plain wordsIn cells, NAP-associated tubulin changes accompanied a larger microtubule network.

    Peptide
    Davunetide
    Outcome
    IncreaseMicrotubule network area
    Study

    ratn: not reported in source

    PC12 cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The effect on tubulin tyrosination/detyrosination was coupled to increased MT network area (measured in PC12 cells), which is directly related to neurite outgrowth.
  4. 04LabIn vitro (cells)Mechanism

    In the cellular study, NAP significantly increased tubulin beta3.

    In plain wordsIn cells, NAP increased tubulin beta3.

    Peptide
    Davunetide
    Outcome
    IncreaseTubulin beta3
    Study

    ratn: not reported in source

    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tubulin beta3, a marker for neurite outgrowth/neuronal differentiation significantly increased after NAP treatment.
  5. 05LabIn vitro (cells)Mechanism

    In rat cortical neurons, NAP doubled dynamic microtubule invasion area in the growth cone periphery.

    In plain wordsIn cells, NAP doubled the area of growing microtubules entering rat neuronal growth cone edges.

    Peptide
    Davunetide
    Outcome
    IncreaseDynamic microtubule invasion area
    Study

    ratn: not reported in source

    Rat cortical neurons
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rat cortical neurons, NAP doubled the area of dynamic MT invasion (Tyr-tubulin) into the neuronal growth cone periphery.
  6. 06LabIn vitro (cells)Mechanism

    In zinc-exposed PC12 cells, NAP reversed the decrease in tau-tubulin-microtubule interaction.

    In plain wordsIn cells exposed to zinc, NAP restored tau interaction with microtubules.

    Peptide
    Davunetide
    Outcome
    IncreaseTau-tubulin-microtubule interaction
    Study

    ratn: not reported in source

    Zinc-exposed PC12 cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    here, in PC12 cells, NAP treatment reversed zinc-decreased tau-tubulin-MT interaction and protected against death.
  7. 07LabIn vitro (cells)Mechanism

    In zinc-exposed PC12 cells, NAP protected against death.

    In plain wordsIn cells exposed to zinc, NAP protected against cell death.

    Peptide
    Davunetide
    Outcome
    DecreaseCell death
    Study

    ratn: not reported in source

    Zinc-exposed PC12 cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    here, in PC12 cells, NAP treatment reversed zinc-decreased tau-tubulin-MT interaction and protected against death.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

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