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Study · In vitro (cells) · 2004

4 results

Thymosin beta 4 and its N-terminal tetrapeptide, AcSDKP, inhibit proliferation, and induce dysplastic, non-apoptotic nuclei and degranulation of mast cells.

Leeanansaksiri W, DeSimone SK, Huff T, Hannappel E, Huff TF

Chemistry & biodiversity1 Jul 2004Cited by 11 (Europe PMC)

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 study4

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

  1. 01LabIn vitro (cells)Activity measurement

    In mast cells, thymosin beta4 inhibited proliferation over 10(-6) to 10(-17) M, with the maximum effect at 10(-14) M.

    In plain wordsIn lab-grown mast cells, thymosin beta4 slowed cell growth across a very wide dose range.

    Outcome
    DecreaseMast-cell proliferation
    Study

    n: not reported in source

    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    10(-6) to 10(-17) MAs given in this study.

    Source sentences

    Summary
    Here, we show that both peptides inhibit mast-cell proliferation over the concentration range of 10(-6) to 10(-17) M with the maximum effect of both at 10(-14) M.
  2. 02LabIn vitro (cells)Activity measurement

    In mast cells, thymosin beta4 caused dysplastic nuclei, confirmed by DAPI fluorescent staining.

    In plain wordsIn lab-grown mast cells, thymosin beta4 caused abnormal cell nuclei.

    Outcome
    IncreaseDysplastic mast-cell nuclei
    Study

    n: not reported in source

    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both Tbeta4 and acSDKP caused dysplastic mast-cell nuclei that were confirmed by DAPI fluorescent staining.
  3. 03LabIn vitro (cells)Mechanism

    In mast cells, flow cytometry showed that the dysplastic nuclei were fragmented nuclei in G2 growth arrest, not multinucleated nuclei.

    In plain wordsIn lab-grown mast cells, the abnormal nuclei were broken nuclei stopped in a growth phase.

    Outcome
    Not applicableNuclear fragmentation and G2 arrest
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Flow-cytometric analysis of ploidy revealed that the dysplastic nuclei were not multinucleated, but fragmented nuclei in G2 growth arrest.
  4. 04LabIn vitro (cells)Activity measurement

    In mast cells, 10(-8) M thymosin beta4 caused 57% degranulation.

    In plain wordsIn lab-grown mast cells, thymosin beta4 made 57% of the cells release their granules.

    Outcome
    IncreaseMast-cell degranulation
    Study

    n: not reported in source

    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    10(-8) MAs given in this study.

    Measurements

    Degranulation
    57%
    10(-8) M Tbeta4

    Source sentences

    Summary
    We could further demonstrate that 10(-8) or 10(-14) M Tbeta4 or acSDKP induce mast-cell degranulation.
    1 context sentence
    Summary · context
    A concentration of 10(-8) M Tbeta4 or acSDKP caused 57 or 89% degranulation, respectively.

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.

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