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Study · In vitro (cells) · mouse · 2002

7 results

Involvement of mitogen-activated protein kinases in the signal transduction pathway of bone marrow-derived macrophage activation in response to in vitro treatment with thymosin alpha 1.

Sodhi A, Paul S

International immunopharmacology1 Jan 2002Cited by 18 (Europe PMC)

PMID11789669 (opens in a new tab)DOI10.1016/s1567-5769(01)00139-4 (opens in a new tab)PepBankPUB-11789669
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

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

  1. 01LabIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, thymosin alpha1 activated phospho-p42/44 MAPK in a dose- and time-dependent way, with a maximum at 5-15 min after 100 ng/ml.

    In plain wordsIn cells from mice, thymosin alpha1 switched on the MAPK signal, with a peak 5 to 15 minutes after treatment.

    Peptide
    Thymosin alpha-1
    Outcome
    IncreasePhospho-p42/44 MAPK activation
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    100 ng/mlAs given in this study (mouse).

    Measurements

    Time to maximum phospho-p42/44 MAPK expression
    5 to 15 min
    100 ng/ml Talpha1

    Source sentences

    Summary
    The activation and expression of phospho-p42/44 MAPK was dose as well as time dependent with maximum expression occurring at 5-15 min following stimulation with 100 ng/ml of Talpha1.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

Studies that did not test the peptide alone6

In this study, Thymosin alpha-1 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 alpha-1.

  1. 02LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, the MAPK inhibitor PD98059 inhibited Talpha1-induced phospho-p42/44 MAPK expression.

    In plain wordsIn cells from mice, the inhibitor PD98059 blocked the MAPK signal that thymosin alpha1 had switched on.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreasePhospho-p42/44 MAPK expression with MAPK inhibitor PD98059
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Receptor activity and mechanism · Immune and inflammation

    Source sentences

    Summary
    The expression of phospho-p42/44 MAPK was inhibited by the MAPK inhibitor, PD98059
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

  2. 03LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, pertussis toxin inhibited Talpha1-induced phospho-p42/44 MAPK expression.

    In plain wordsIn cells from mice, pertussis toxin blocked the MAPK signal that thymosin alpha1 had switched on.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreasePhospho-p42/44 MAPK expression with pertussis toxin
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Receptor activity and mechanism · Immune and inflammation

    Source sentences

    Summary
    The expression of phospho-p42/44 MAPK was inhibited by the MAPK inhibitor, PD98059, pertussis toxin (PTX), tyrosine kinase inhibitor-genistein and P13K inhibitor-wortmannin.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

  3. 04LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, the tyrosine kinase inhibitor genistein inhibited Talpha1-induced phospho-p42/44 MAPK expression.

    In plain wordsIn cells from mice, genistein blocked the MAPK signal that thymosin alpha1 had switched on.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreasePhospho-p42/44 MAPK expression with genistein
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Receptor activity and mechanism · Immune and inflammation

    Source sentences

    Summary
    The expression of phospho-p42/44 MAPK was inhibited by the MAPK inhibitor, PD98059, pertussis toxin (PTX), tyrosine kinase inhibitor-genistein and P13K inhibitor-wortmannin.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

  4. 05LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, the inhibitor wortmannin inhibited Talpha1-induced phospho-p42/44 MAPK expression.

    In plain wordsIn cells from mice, wortmannin blocked the MAPK signal that thymosin alpha1 had switched on.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreasePhospho-p42/44 MAPK expression with wortmannin
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Receptor activity and mechanism · Immune and inflammation

    Source sentences

    Summary
    The expression of phospho-p42/44 MAPK was inhibited by the MAPK inhibitor, PD98059, pertussis toxin (PTX), tyrosine kinase inhibitor-genistein and P13K inhibitor-wortmannin.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

  5. 06LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, the MAPK inhibitor PD98059 inhibited Talpha1-induced nitric oxide production in a dose-dependent manner.

    In plain wordsIn cells from mice, the inhibitor PD98059 reduced nitric oxide made after thymosin alpha1 treatment.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreaseTalpha1-induced nitric oxide production with PD98059
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Immune response · Immune and inflammation

    Source sentences

    Summary
    Talpha1-induced BMDM tumoricidal functions like the production of NO and TNF-alpha, the key mediator molecules of macrophage cytotoxicity, were also inhibited by the MAPK inhibitor, PD98059, in a dose-dependent manner.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

  6. 07LabNot a test of Thymosin alpha-1 aloneIn vitro (cells)Mechanism

    In murine bone marrow-derived macrophages, the MAPK inhibitor PD98059 inhibited Talpha1-induced TNF-alpha production in a dose-dependent manner.

    In plain wordsIn cells from mice, the inhibitor PD98059 reduced TNF-alpha made after thymosin alpha1 treatment.

    Peptide
    Thymosin alpha-1
    Outcome
    DecreaseTalpha1-induced TNF-alpha production with PD98059
    Study

    mousen: not reported in source

    Murine bone marrow-derived macrophages (BMDMs)
    Outcome group
    Immune response · Immune and inflammation

    Source sentences

    Summary
    Talpha1-induced BMDM tumoricidal functions like the production of NO and TNF-alpha, the key mediator molecules of macrophage cytotoxicity, were also inhibited by the MAPK inhibitor, PD98059, in a dose-dependent manner.
    1 context sentence
    Summary · context
    In the present investigation, the activation of the p42/44 MAP kinase (MAPK)/c-Jun NH2 terminal kinase (JNK) pathway in response to in vitro treatment with Talpha1 in murine bone marrow-derived macrophages (BMDMs) has been demonstrated.

    In this study, Thymosin alpha-1 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 alpha-1.

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 3Current

    10 Oct 2026, 08:55 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 03:02 UTC

    First added · source update from Europe PMC

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Terms as the source lists them.

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