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Study · In vitro (cells) · 2019

7 results

Thymosin beta 4-Induced Autophagy Increases Cholinergic Signaling in PrP (106-126)-Treated HT22 Cells.

Han HJ, Kim S, Kwon J

Neurotoxicity research15 Dec 2018Cited by 5 (Europe PMC)

PMID30552633 (opens in a new tab)DOI10.1007/s12640-018-9985-0 (opens in a new tab)PepBankPUB-30552633
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

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

  1. 01LabIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, Tβ4 induced the autophagy marker LC3A/B, which was protective against PrP-induced neurotoxicity.

    In plain wordsIn cells, thymosin beta‑4 raised the autophagy marker LC3A/B, which protected against prion peptide toxicity.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseLC3A/B autophagy marker
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that Tβ4-induced autophagy markers, LC3A/B and Beclin1, were protective against PrP-induced neurotoxicity.
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.
  2. 02LabIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, Tβ4 induced the autophagy marker Beclin1, which was protective against PrP-induced neurotoxicity.

    In plain wordsIn cells, thymosin beta‑4 raised the autophagy marker Beclin1, which protected against prion peptide toxicity.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseBeclin1 autophagy marker
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that Tβ4-induced autophagy markers, LC3A/B and Beclin1, were protective against PrP-induced neurotoxicity.
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.
  3. 03LabIn vitro (cells)Efficacy outcome

    In PrP (106-126)-treated HT22 cells, Tβ4-induced autophagy markers were protective against PrP-induced neurotoxicity.

    In plain wordsIn cells, thymosin beta‑4 protected against toxicity from a prion protein peptide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreasePrP-induced neurotoxicity
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that Tβ4-induced autophagy markers, LC3A/B and Beclin1, were protective against PrP-induced neurotoxicity.
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.
  4. 04LabIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, Tβ4 maintained a balance between autophagy markers and the pathway factors AKT, p-AKT, mTOR and p-mTOR against the effect of PrP (106-126).

    In plain wordsIn cells, thymosin beta‑4 kept autophagy pathway proteins in balance against the effect of a prion protein peptide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableAutophagy pathway factors (AKT, p-AKT, mTOR, p-mTOR)
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, a balance between autophagy markers and autophagy pathway factors (AKT, p-AKT, mTOR, and p-mTOR) was maintained by Tβ4 competitively against each protein factors reacted to PrP (106-126).
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.
  5. 05LabIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, Tβ4 maintained the cholinergic signaling marker ChTp against the effect of PrP (106-126).

    In plain wordsIn cells, thymosin beta‑4 kept the cholinergic marker ChTp stable against the effect of a prion protein peptide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableCholinergic marker ChTp
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The cholinergic signaling markers ChTp and AChE, which play an important role in the brain, were maintained by Tβ4 competitively against each protein factors reacted to PrP (106-126).
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.
  6. 06LabIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, Tβ4 maintained the cholinergic signaling marker AChE against the effect of PrP (106-126).

    In plain wordsIn cells, thymosin beta‑4 kept the cholinergic marker AChE stable against the effect of a prion protein peptide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableCholinergic marker AChE
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    PrP (106-126)-treated cells
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The cholinergic signaling markers ChTp and AChE, which play an important role in the brain, were maintained by Tβ4 competitively against each protein factors reacted to PrP (106-126).
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.

Studies that did not test the peptide alone1

In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Thymosin beta-4 (human).

  1. 07LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In PrP (106-126)-treated HT22 cells, the autophagy inhibitor 3-MA reversed the Tβ4 effects on autophagy and cholinergic markers.

    In plain wordsIn cells, an autophagy blocker reversed the effects that thymosin beta‑4 had on autophagy and cholinergic markers.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableTβ4 effects with autophagy inhibitor 3-MA
    Study

    n: not reported in source

    PrP (106-126)-treated HT22 cells
    Comparator
    Tβ4 without 3-MA
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    However, these results were reversed by 3-MA, an autophagy inhibitor.
    1 context sentence
    Summary · context
    In this study, we investigated the neuroprotective effects of Tβ4, an activator of autophagy, in cholinergic signaling activation in PrP (106-126)-treated HT22 cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

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

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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