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Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Updated: May 10, 2026

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
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Published on: April 24, 2021

Crosstalk between ER stress and immunogenic cell death.

Oliver Kepp1, Laurie Menger, Erika Vacchelli

  • 1Université Paris-Sud/Paris XI, Le Kremlin-Bicêtre, France; INSERM, U848, Villejuif, France; Institut Gustave Roussy, Villejuif, France.

Cytokine & Growth Factor Reviews
|June 22, 2013
PubMed
Summary

Therapeutic regimens using immunogenic cell death (ICD) inducers show clinical success due to tumor-specific immune responses. Endoplasmic reticulum (ER) stress pathways are key to ICD induction and represent potential cancer therapy targets.

Keywords:
ATPAnthracyclinesApoptosisCalciumCalreticulinPERK

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Therapeutic regimens utilizing immunogenic cell death (ICD) inducers like anthracyclines and oxaliplatin demonstrate clinical efficacy, partly attributed to tumor-specific immune responses.
  • The precise molecular mechanisms by which certain cytotoxic agents induce ICD are not fully understood.
  • The endoplasmic reticulum (ER) stress response is consistently implicated in all observed ICD scenarios.

Purpose of the Study:

  • To review recent advancements in immunogenic cell death (ICD) research.
  • To highlight the critical role of endoplasmic reticulum (ER) stress in ICD.
  • To explore the therapeutic implications of ER stress-induced ICD in cancer treatment.

Main Methods:

  • Literature review of preclinical and clinical studies on ICD inducers.
  • Analysis of molecular pathways involved in cytotoxic agent-induced cell death.
  • Focus on the endoplasmic reticulum (ER) stress response mechanisms.

Main Results:

  • Tumor-specific immune responses correlate with the success of ICD-inducing therapies.
  • Endoplasmic reticulum (ER) stress is a common pathway across different ICD inducers.
  • Components of the ER stress machinery are potential druggable targets for enhancing ICD.

Conclusions:

  • The endoplasmic reticulum (ER) stress response is central to immunogenic cell death (ICD).
  • Targeting ER stress pathways offers a promising strategy for novel cancer immunotherapies.
  • Further research into ER stress mechanisms can optimize ICD-based cancer treatments.