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The **ER stress pathway** comprises molecular sensors in the endoplasmic reticulum (PERK, IRE1, ATF6) that detect protein misfolding and initiate the **unfolded protein response (UPR)**, an adaptive mechanism to restore proteostasis or trigger apoptosis if the stress is prolonged. These pathways are major regulators of cell fate. Their dysfunction contributes to diverse diseases, and their components (particularly PERK, IRE1, and ATF6) are being actively investigated as therapeutic targets, especially in oncology, metabolic disorders, and neurodegeneration. The pathway integrates **protein synthesis regulation**, **apoptosis induction**, **autophagy**, and **inflammatory signaling**, with numerous downstream effectors that may serve as drug targets or disease biomarkers.
Inhibition or modulation of UPR sensors (e.g., kinase inhibitors targeting PERK, IRE1); Chemical chaperone-mediated alleviation of protein misfolding; Blocking apoptosis or autophagy downstream of ER stress; Restoration of ER homeostasis
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See how Gosset can support your research on Endoplasmic reticulum stress pathway components (ER stress pathway (no standardized abbreviation for the entire set; components are typically abbreviated as PERK, IRE1, ATF6, etc.)).