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A UPR-Induced Soluble ER-Phagy Receptor Acts with VAPs to Confer ER Stress Resistance
A Stress-Activated Receptor Helps Clear Cell Factories to Protect Against Protein-Build-Up Stress
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Abstract
ER-phagy is required for survival during ER stress in the fission yeast Schizosaccharomyces pombe.
- ER-phagy is triggered by stress in the endoplasmic reticulum (ER).
- Epr1 is a key receptor that interacts with Atg8 and is essential for ER-phagy.
- Epr1 connects Atg8 to integral membrane proteins known as VAPs, facilitating ER-phagy.
- VAPs not only tether Atg8 to the ER but also help maintain contact between the ER and plasma membrane.
- Epr1 levels increase in response to ER stress signals from the unfolded protein response regulator Ire1.
- Reducing Epr1 expression decreases survival chances during periods of ER stress.
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