Skip to content

Study · In vitro (cells) · 2013

6 results

G-actin sequestering protein thymosin-β4 regulates the activity of myocardin-related transcription factor.

Morita T, Hayashi K

Biochemical and biophysical research communications28 Jun 2013Cited by 12 (Europe PMC)

PMID23811404 (opens in a new tab)DOI10.1016/j.bbrc.2013.06.069 (opens in a new tab)PepBankPUB-23811404
Publisher pagePubMedAsk about this study
Jump to 6 results

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 study6

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

  1. 01LabIn vitro (cells)Mechanism

    In cells, Tβ4 competed with MRTF-A for G-actin binding and so interfered with formation of the G-actin-MRTF-A complex.

    In plain wordsIn cells, Tβ4 competed with MRTF-A for actin binding and so reduced the actin-MRTF-A complex.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableTβ4 competition with MRTF-A for G-actin
    Study

    n: not reported in source

    living cells
    Outcome group
    Receptor activity and mechanism · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 competed with MRTF-A for G-actin binding; thus, interfering with G-actin-MRTF-A complex formation.
    1 context sentence
    Summary · context
    Here, we demonstrate that the most abundant G-actin sequestering protein thymosin-β4 (Tβ4) was involved in the regulation of subcellular localization and activity of MRTF-A.

Studies that did not test the peptide alone5

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. 02LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, Tβ4 overexpression induced nuclear accumulation of MRTF-A.

    In plain wordsIn cells, raising Tβ4 gene activity moved more MRTF-A protein into the cell nucleus.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseMRTF-A nuclear accumulation
    Study

    n: not reported in source

    living cells
    Outcome group
    Receptor activity and mechanism · Whole body

    Source sentences

    Summary
    Tβ4 overexpression induced the MRTF-A nuclear accumulation and activation of MRTF-SRF signaling.

    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. 03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, Tβ4 overexpression activated MRTF-SRF signaling.

    In plain wordsIn cells, raising Tβ4 gene activity switched on MRTF-SRF signaling.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseMRTF-SRF signaling activation
    Study

    n: not reported in source

    living cells
    Outcome group
    Receptor activity and mechanism · Whole body

    Source sentences

    Summary
    Tβ4 overexpression induced the MRTF-A nuclear accumulation and activation of MRTF-SRF signaling.

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

    In cells, ectopic Tβ4 increased the endogenous expression of SRF-dependent actin cytoskeletal genes.

    In plain wordsIn cells, extra Tβ4 made inside the cell increased the activity of the cells' own SRF-dependent actin genes.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseEndogenous SRF-dependent actin cytoskeletal gene expression
    Study

    n: not reported in source

    living cells
    Outcome group
    Receptor activity and mechanism · Whole body

    Source sentences

    Summary
    Furthermore, ectopic Tβ4 increased the endogenous expression of SRF-dependent actin cytoskeletal genes.

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

    In cells, the Tβ4 mutant L17A, which has very low affinity for G-actin, activated MRTF-A less than wild-type Tβ4.

    In plain wordsIn cells, a Tβ4 mutant with weak actin binding switched on MRTF-A less than normal Tβ4.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseMRTF-A activation by Tβ4 mutant L17A
    Study

    n: not reported in source

    living cells
    Comparator
    Wild-type Tβ4
    Outcome group
    Receptor activity and mechanism · Whole body

    Source sentences

    Summary
    The activation rate of MRTF-A by the Tβ4 mutant L17A, whose affinity for G-actin is very low, was lower than that by wild-type Tβ4.

    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).

  5. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cells, the β-actin mutant 3DA, which has lower affinity for Tβ4, suppressed MRTF-A activity more effectively than wild-type β-actin.

    In plain wordsIn cells, an actin mutant that binds Tβ4 less well blocked MRTF-A more than normal actin.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseMRTF-A suppression by β-actin mutant 3DA
    Study

    n: not reported in source

    living cells
    Comparator
    Wild-type β-actin
    Outcome group
    Receptor activity and mechanism · Whole body

    Source sentences

    Summary
    In contrast, the β-actin mutant 3DA, which has a lower affinity for Tβ4, more effectively suppressed MRTF-A activity than wild-type β-actin.

    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.

PepBank is a research reference. Talk to a doctor before you use any peptide.