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Study · In vitro (cells) · 2008

12 results

Ku80 as a novel receptor for thymosin beta4 that mediates its intracellular activity different from G-actin sequestering.

Bednarek R, Boncela J, Smolarczyk K, Cierniewska-Cieslak A, Wyroba E, Cierniewski CS

The Journal of biological chemistry4 Nov 2007Cited by 33 (Europe PMC)

PMID17984099 (opens in a new tab)DOI10.1074/jbc.m707539200 (opens in a new tab)PepBankPUB-17984099
Publisher pagePubMedAsk about this study
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Summary

Our data demonstrate that increased intracellular expression of thymosin beta4(Tbeta4) is necessary and sufficient to induce plasminogen activator inhibitor type 1 (PAI-1) gene expression in endothelial cells. To describe the mechanism of this effect, we produced Tbeta4 mutants with impaired functional motifs and tested their intracellular location and activity. Cytoplasmic distributions of Tbeta4((AcSDKPT/4A)), Tbeta4((KLKKTET/7A)), and Tbeta4((K16A)) mutants fused with green fluorescent protein did not differ significantly from those of wild-type Tbeta4. Overexpression of Tbeta4, Tbeta4((AcSDKPT/4A)), and Tbeta4((K16A)) affected intracellular formation of actin filaments. As expected, Tbeta4((K16A)) uptake by nuclei was impaired. On the other hand, overexpression of Tbeta4((KLKKTET/7A)) resulted in developing the actin filament network typical of adhering cells, indicating that the mutant lacked the actin binding site. The mechanism by which intracellular Tbeta4 induced the PAI-1 gene did not depend upon the N-terminal tetrapeptide AcSDKP and depended only partially on its ability to bind G-actin or enter the nucleus. Both Tbeta4 and Tbeta4((AcSDKPT/4A)) induced the PAI-1 gene to the same extent, whereas mutants Tbeta4((KLKKTET/7A)) and Tbeta4((K16A)) retained about 60% of the original activity. By proteomic analysis, the Ku80 subunit of ATP-dependent DNA helicase II was found to be associated with Tbeta4. Ku80 and Tbeta4 consistently co-immunoprecipitated in a complex from endothelial cells. Co-transfection of endothelial cells with the Ku80 deletion mutants and Tbeta4 showed that the C-terminal arm domain of Ku80 is directly involved in this interaction. Furthermore, down-regulation of Ku80 by specific short interference RNA resulted in dramatic reduction in PAI-1 expression at the level of both mRNA and protein synthesis. These data suggest that Ku80 functions as a novel receptor for Tbeta4 and mediates its intracellular activity.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study12

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

  1. 01LabIn vitro (cells)Activity measurement

    By proteomic analysis, the Ku80 subunit of ATP-dependent DNA helicase II was found to be associated with thymosin beta4.

    In plain wordsIn lab tests, a protein called Ku80 was found to be linked with thymosin beta4.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableKu80 association with Tbeta4 by proteomic analysis
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    By proteomic analysis, the Ku80 subunit of ATP-dependent DNA helicase II was found to be associated with Tbeta4.
  2. 02LabIn vitro (cells)Activity measurement

    In endothelial cells, Ku80 and thymosin beta4 co-immunoprecipitated in a complex.

    In plain wordsIn cells, Ku80 and thymosin beta4 were found together in one complex.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableKu80 and Tbeta4 co-immunoprecipitation
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ku80 and Tbeta4 consistently co-immunoprecipitated in a complex from endothelial cells.
  3. 03LabIn vitro (cells)Mechanism

    In endothelial cells, the C-terminal arm domain of Ku80 was directly involved in the interaction with thymosin beta4.

    In plain wordsIn cells, one end part of Ku80 took part directly in the contact with thymosin beta4.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableKu80 domain involved in Tbeta4 interaction
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-transfection of endothelial cells with the Ku80 deletion mutants and Tbeta4 showed that the C-terminal arm domain of Ku80 is directly involved in this interaction.

Studies that did not test the peptide alone9

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 endothelial cells, increased intracellular thymosin beta4 was necessary and sufficient to induce PAI-1 gene expression.

    In plain wordsIn blood vessel lining cells, raising Tβ4 inside the cells was enough to switch on the PAI-1 gene.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreasePAI-1 gene expression
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Our data demonstrate that increased intracellular expression of thymosin beta4(Tbeta4) is necessary and sufficient to induce plasminogen activator inhibitor type 1 (PAI-1) gene expression in endothelial 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).

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

    In endothelial cells, overexpression of thymosin beta4 affected intracellular formation of actin filaments.

    In plain wordsIn blood vessel lining cells, raising Tβ4 gene activity changed how actin filaments formed inside the cells. The direction is not stated.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Direction not reportedIntracellular actin filament formation
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Overexpression of Tbeta4, Tbeta4((AcSDKPT/4A)), and Tbeta4((K16A)) affected intracellular formation of actin filaments.

    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 endothelial cells, siRNA down-regulation of Ku80 sharply reduced PAI-1 mRNA expression.

    In plain wordsIn cells, lowering Ku80 strongly reduced PAI-1 mRNA.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseKu80 knockdown effect on PAI-1 mRNA
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Furthermore, down-regulation of Ku80 by specific short interference RNA resulted in dramatic reduction in PAI-1 expression at the level of both mRNA and protein synthesis.

    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 endothelial cells, siRNA down-regulation of Ku80 sharply reduced PAI-1 protein synthesis.

    In plain wordsIn cells, lowering Ku80 strongly reduced PAI-1 protein.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseKu80 knockdown effect on PAI-1 protein synthesis
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Furthermore, down-regulation of Ku80 by specific short interference RNA resulted in dramatic reduction in PAI-1 expression at the level of both mRNA and protein synthesis.

    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. 08LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Activity measurement

    In endothelial cells, the Tbeta4 AcSDKPT/4A mutant induced the PAI-1 gene to the same extent as wild-type Tbeta4.

    In plain wordsIn cells, a changed form of thymosin beta4 switched on the PAI-1 gene as much as the normal form.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    No significant changePAI-1 induction by Tbeta4 AcSDKPT/4A mutant
    Study

    n: not reported in source

    endothelial cells
    Comparator
    Wild-type Tbeta4
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Both Tbeta4 and Tbeta4((AcSDKPT/4A)) induced the PAI-1 gene to the same extent, whereas mutants Tbeta4((KLKKTET/7A)) and Tbeta4((K16A)) retained about 60% of the original activity.

    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).

  6. 09LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Activity measurement

    In endothelial cells, the Tbeta4 KLKKTET/7A and K16A mutants retained about 60% of the original PAI-1 inducing activity.

    In plain wordsIn cells, two changed forms of thymosin beta4 kept about 60% of the normal activity.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreasePAI-1 induction by Tbeta4 KLKKTET/7A and K16A mutants
    Study

    n: not reported in source

    endothelial cells
    Comparator
    Wild-type Tbeta4
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Measurements

    PAI-1 induction activity retained
    ≈ 60%
    KLKKTET/7A and K16A mutants

    Source sentences

    Summary
    Both Tbeta4 and Tbeta4((AcSDKPT/4A)) induced the PAI-1 gene to the same extent, whereas mutants Tbeta4((KLKKTET/7A)) and Tbeta4((K16A)) retained about 60% of the original activity.

    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).

  7. 10LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Activity measurement

    In endothelial cells, the cytoplasmic distributions of three GFP-fused Tbeta4 mutants did not differ significantly from wild-type Tbeta4.

    In plain wordsIn cells, three changed forms of thymosin beta4 spread in the cell fluid like the normal form.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    No significant changeCytoplasmic distribution of Tbeta4 mutants
    Study

    n: not reported in source

    endothelial cells
    Comparator
    Wild-type Tbeta4
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Cytoplasmic distributions of Tbeta4((AcSDKPT/4A)), Tbeta4((KLKKTET/7A)), and Tbeta4((K16A)) mutants fused with green fluorescent protein did not differ significantly from those of wild-type Tbeta4.

    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).

  8. 11LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Activity measurement

    In endothelial cells, uptake of the Tbeta4 K16A mutant by nuclei was impaired.

    In plain wordsIn cells, one changed form of thymosin beta4 entered the nucleus less well.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseNuclear uptake of Tbeta4 K16A mutant
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    As expected, Tbeta4((K16A)) uptake by nuclei was impaired.

    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).

  9. 12LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In endothelial cells, overexpression of the Tbeta4 KLKKTET/7A mutant produced the actin filament network typical of adhering cells, indicating loss of the actin binding site.

    In plain wordsIn cells, a changed form of thymosin beta4 lacking the actin binding site led to an actin network typical of adhering cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Direction not reportedActin filament network with Tbeta4 KLKKTET/7A mutant
    Study

    n: not reported in source

    endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    On the other hand, overexpression of Tbeta4((KLKKTET/7A)) resulted in developing the actin filament network typical of adhering cells, indicating that the mutant lacked the actin binding site.

    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

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