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Endoplasmic reticulum stress responses.

M Schröder1

  • 1School of Biological and Biomedical Sciences, Durham University, Durham, UK. martin.schroeder@durham.ac.uk

Cellular and Molecular Life Sciences : CMLS
|November 27, 2007
PubMed
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Cellular stress disrupts homeostasis. This review explains how endoplasmic reticulum (ER) stress activates the unfolded protein response (UPR) to restore balance, influencing cell survival and inflammation.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Physiology

Background:

  • Cellular homeostasis relies on dynamic equilibrium.
  • Disruptions to homeostasis lead to cellular stress.
  • The endoplasmic reticulum (ER) is crucial for cellular functions.

Purpose of the Study:

  • To review how ER functional perturbations induce ER stress.
  • To explain the activation and function of the unfolded protein response (UPR).
  • To summarize the control of UPR signaling transitions and inflammatory induction.

Main Methods:

  • Literature review of ER stress and UPR.
  • Analysis of signaling pathways involved in UPR.
  • Synthesis of current understanding on UPR regulation.

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Main Results:

  • Perturbation of ER protein folding, lipid biosynthesis, or Ca(2+) storage causes ER stress.
  • ER stress activates the UPR to reestablish homeostasis.
  • UPR signaling transitions from protective to apoptotic pathways are controlled.
  • UPR signaling can induce inflammatory responses.

Conclusions:

  • The UPR is a critical adaptive response to ER stress.
  • Understanding UPR control is key to managing cellular stress and inflammation.
  • ER stress and UPR are central to cellular health and disease.