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Study · In vitro (cells) · mouse · 2015

7 results

Modulation of cellular stress response via the erythropoietin/CD131 heteroreceptor complex in mouse mesenchymal-derived cells.

Bohr S, Patel SJ, Vasko R, Shen K, Iracheta-Vellve A, Lee J, Bale SS, Chakraborty N, Brines M, Cerami A, Berthiaume F, Yarmush ML

Journal of molecular medicine (Berlin, Germany)6 Nov 2014Cited by 25 (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 study7

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

  1. 01LabIn vitro (cells)Mechanism

    In mouse mesenchymal-derived cells, the effects of ARA290 and EPO coincided with externalization of the CD131 receptor component as an immediate response to cellular stress.

    In plain wordsIn mouse cells in lab tests, ARA290 effects occurred together with CD131 moving to the cell surface under stress.

    Outcome
    IncreaseCD131 externalization with ARA290 and EPO effects
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We show that anti-apoptotic, anti-inflammatory effects of ARA290 and EPO coincide with the externalization of CD131 receptor component as an immediate response to cellular stress.
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  2. 02LabIn vitro (cells)Efficacy outcome

    In mouse mesenchymal-derived cells, ARA290 had anti-apoptotic effects under cellular stress.

    In plain wordsIn mouse cells in lab tests, ARA290 protected stressed cells from programmed cell death.

    Outcome
    DecreaseAnti-apoptotic effect
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We show that anti-apoptotic, anti-inflammatory effects of ARA290 and EPO coincide with the externalization of CD131 receptor component as an immediate response to cellular stress.
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  3. 03LabIn vitro (cells)Efficacy outcome

    In mouse mesenchymal-derived cells, ARA290 had anti-inflammatory effects under cellular stress.

    In plain wordsIn mouse cells in lab tests, ARA290 reduced inflammation in stressed cells.

    Outcome
    DecreaseAnti-inflammatory effect
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We show that anti-apoptotic, anti-inflammatory effects of ARA290 and EPO coincide with the externalization of CD131 receptor component as an immediate response to cellular stress.
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  4. 04LabIn vitro (cells)Efficacy outcome

    In mouse mesenchymal-derived cells, ARA290 overcame the TNFα-mediated inhibition of serum response factor activation.

    In plain wordsIn mouse cells in lab tests, ARA290 reversed the block that TNFα placed on the stress-response factor SRF.

    Outcome
    IncreaseSRF activation after TNFα inhibition
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Specifically, we saw that ARA290 was able to overcome a TNFα-mediated inhibition of transcription factor activation related to cell stress responses, most notably of serum response factor (SRF), heat shock transcription factor protein 1 (HSF1), and activator protein 1 (AP1).
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  5. 05LabIn vitro (cells)Efficacy outcome

    In mouse mesenchymal-derived cells, ARA290 overcame the TNFα-mediated inhibition of heat shock transcription factor 1 activation.

    In plain wordsIn mouse cells in lab tests, ARA290 reversed the block that TNFα placed on the stress-response factor HSF1.

    Outcome
    IncreaseHSF1 activation after TNFα inhibition
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Specifically, we saw that ARA290 was able to overcome a TNFα-mediated inhibition of transcription factor activation related to cell stress responses, most notably of serum response factor (SRF), heat shock transcription factor protein 1 (HSF1), and activator protein 1 (AP1).
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  6. 06LabIn vitro (cells)Efficacy outcome

    In mouse mesenchymal-derived cells, ARA290 overcame the TNFα-mediated inhibition of activator protein 1 activation.

    In plain wordsIn mouse cells in lab tests, ARA290 reversed the block that TNFα placed on the stress-response factor AP1.

    Outcome
    IncreaseAP1 activation after TNFα inhibition
    Study

    mousen: not reported in source

    mesenchymal-derived cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Specifically, we saw that ARA290 was able to overcome a TNFα-mediated inhibition of transcription factor activation related to cell stress responses, most notably of serum response factor (SRF), heat shock transcription factor protein 1 (HSF1), and activator protein 1 (AP1).
    1 context sentence
    Summary · context
    In this study, we investigated effects of signaling through EPO-R/CD131 complex on cellular stress responses and pro-inflammatory activation in different mesenchymal-derived phenotypes.
  7. 07LabIn vitro (cells)Activity measurement

    ARA290 peptide specifically binds the EPO/CD131 receptor but not the canonical EPO/EPO receptor.

    In plain wordsIn lab tests, ARA290 binds the EPO/CD131 receptor pair and does not bind the usual EPO/EPO receptor.

    Outcome
    Not applicableBinding specificity of ARA290 (EPO/CD131 vs canonical EPO/EPO receptor)
    Study

    n: not reported in source

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

    Source sentences

    Summary
    ARA290 peptide specifically binds EPO/CD131 but not the canonical EPO/EPO receptor.

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

    9 Oct 2026, 19:08 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:13 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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