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Study · In vitro (cells) · 2018

3 results

AMPK alleviates endoplasmic reticulum stress by inducing the ER-chaperone ORP150 via FOXO1 to protect human bronchial cells from apoptosis.

Liu JQ, Zhang L, Yao J, Yao S, Yuan T

Biochemical and biophysical research communications12 Feb 2018Cited by 38 (Europe PMC)

PMID29448096 (opens in a new tab)DOI10.1016/j.bbrc.2018.02.095 (opens in a new tab)PepBankPUB-29448096
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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 study3

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In human bronchial epithelial cells exposed to cigarette smoke extract, AICAR reduced ER stress-induced apoptosis.

    In plain wordsIn cells exposed to cigarette smoke extract, AICAR reduced stress-induced cell death.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseER stress-induced apoptosis
    Study

    humann: not reported in source

    Human bronchial epithelial cells
    Outcome group
    Cell viability and death · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, co-treatment with N1-(β-d-ribofuranosyl)-5-aminoimidazole-4-carboxamide (AICAR), a pharmacological activator of AMPK, significantly increased cell protection against ER stress-induced apoptosis
  2. 02LabIn vitro (cells)Mechanism

    In human bronchial epithelial cells, AICAR increased ORP150 expression.

    In plain wordsIn cells, AICAR increased ORP150 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseORP150 expression
    Study

    humann: not reported in source

    Human bronchial epithelial cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by upregulating the 150 kDa oxygen-regulated protein (ORP150), which functions as an ER-associated chaperone, with concomitant elevation of FOXO1, a critical transcription factor regulating ORP150 expression.
  3. 03LabIn vitro (cells)Mechanism

    In human bronchial epithelial cells, AICAR increased FOXO1 expression.

    In plain wordsIn cells, AICAR increased FOXO1 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseFOXO1 expression
    Study

    humann: not reported in source

    Human bronchial epithelial cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by upregulating the 150 kDa oxygen-regulated protein (ORP150), which functions as an ER-associated chaperone, with concomitant elevation of FOXO1, a critical transcription factor regulating ORP150 expression.

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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