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Study · In vitro (cells) · 2011

7 results

Thymosin beta4 inhibits TNF-alpha-induced NF-kappaB activation, IL-8 expression, and the sensitizing effects by its partners PINCH-1 and ILK.

Qiu P, Wheater MK, Qiu Y, Sosne G

FASEB journal : official publication of the Federation of American Societies for Experimental Biology22 Feb 2011Cited by 84 (Europe PMC)

PMID21343177 (opens in a new tab)PMCIDPMC3101037 (opens in a new tab)DOI10.1096/fj.10-167940 (opens in a new tab)PepBankPUB-21343177
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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

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

  1. 01LabIn vitro (cells)Mechanism

    In cells, thymosin beta‑4 directly targeted the NF-kB RelA/p65 subunit.

    In plain wordsIn cells, thymosin beta‑4 acted directly on a key part of the NF-kB inflammation pathway.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableDirect targeting of NF-kB RelA/p65 subunit
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Herein, we present novel evidence that Tβ(4) directly targets the NF-κB RelA/p65 subunit.
  2. 02LabIn vitro (cells)Mechanism

    In cells, the inhibition of NF-kB activation and IL-8 transcription by thymosin beta‑4 was independent of its G-actin-binding properties.

    In plain wordsIn cells, thymosin beta‑4 reduced NF-kB activity without needing its actin-binding function.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableDependence on G-actin binding
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    These activities are independent of the G-actin-binding properties of Tβ(4).
  3. 03LabIn vitro (cells)Mechanism

    In cells, thymosin beta‑4 inhibited the sensitizing effects of PINCH-1 and ILK on NF-kB activity after TNF-alpha stimulation.

    In plain wordsIn cells, thymosin beta‑4 blocked the way PINCH-1 and ILK increase NF-kB activity after TNF-alpha.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseSensitizing effect of PINCH-1 and ILK on NF-kB activity
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ(4) also inhibits the sensitizing effects of its intracellular binding partners, PINCH-1 and ILK, on NF-κB activity after TNF-α stimulation.

Studies that did not test the peptide alone4

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. 04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, enforced expression of thymosin beta‑4 interfered with TNF-alpha-mediated NF-kB activation.

    In plain wordsIn cells, forcing high Tβ4 gene activity interfered with TNF-alpha switching on NF-kB.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseTNF-alpha-mediated NF-kB activation
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    We find that enforced expression of Tβ(4) interferes with TNF-α-mediated NF-κB activation, as well as downstream IL-8 gene transcription.

    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).

  2. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, enforced expression of thymosin beta‑4 interfered with downstream IL-8 gene transcription after TNF-alpha stimulation.

    In plain wordsIn cells, forcing high Tβ4 gene activity reduced switching on of the IL-8 gene after TNF-alpha.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseDownstream IL-8 gene transcription
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    We find that enforced expression of Tβ(4) interferes with TNF-α-mediated NF-κB activation, as well as downstream IL-8 gene transcription.

    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).

  3. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, thymosin beta‑4 blocked nuclear translocation of RelA/p65.

    In plain wordsIn cells with high Tβ4 made inside them, the NF-kB subunit RelA/p65 was blocked from moving into the nucleus.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseRelA/p65 nuclear translocation
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Tβ(4) blocks RelA/p65 nuclear translocation and targeting to the cognate κB site in the proximal region of the IL-8 gene promoter.

    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).

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

    In cells, thymosin beta‑4 blocked targeting of RelA/p65 to the kB site in the proximal region of the IL-8 gene promoter.

    In plain wordsIn cells with high Tβ4 made inside them, RelA/p65 was blocked from reaching its binding site on the IL-8 gene.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseRelA/p65 targeting to kB site of IL-8 promoter
    Study

    n: not reported in source

    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Tβ(4) blocks RelA/p65 nuclear translocation and targeting to the cognate κB site in the proximal region of the IL-8 gene promoter.

    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.

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